Emotional arousal can alter both attentional focus and consolidation of memories.

• If it acts on consolidation, its effect should magnify following a delay (since consolidation occurs over time)
• When arousal is manipulated at encoding and recall is probed at multiple retention intervals, material learned under high arousal is retained better after a delay than immediately following encoding (Eysenck, 1976; Heuer & Reisberg, 1992).
• What’s the mechanism mediating this phenomenon?
  • Animal studies implicate the amygdala – direct interconnections with hippocampus and indirect feedback via peripheral hormone release

STUDY

Methods

• Subjects had unilateral resection of anteromedial temporal lobe (amygdala, hippcampus, adjacent cortex). Good for examining amygdalo-hippocampal system without severe amnesia from bilateral hippocampal damage. Some subjects had left temporal lobe (LTL) resections and some had right.
• 3 groups: Control, LTL, RTL
• During encoding, subjects were shown arousing and neutral words while SCRs and arousal ratings were recorded. RTs also recorded for arousal ratings. Familiarity ratings also recorded.

Results

• No significant group differences at encoding – all groups showed less familiarity, longer RTs and higher SCRs for arousing words
• But when retention was studied, 3-way interaction between group, word type, and retention interval
  • Only controls displayed differential forgetting rates for arousing vs. neutral words (sig increase in recall for arousing words over time)
  • Temporal-lobectomy groups showed no forgetting-resistant memory traces for arousing words (i.e. impaired consolidation)
  • Main effect of hemisphere; hemisphere x word interaction: LTL had lower recall levels, especially for taboo words
  • To show that control performance was not related to initial levels of recall, median split to separate low vs. high recall level. Threeway within control (recall level x word category x retention level) was n.s. Thus, influence of arousal on forgetting rate not related to individual differences in initial recall level within controls.

Discussion

• Amygdala strengthens hippocampal-dependent memory during postencoding time window for both animals and humans
• Alternative explanations for temporal influences of arousal on memory: differences in rehearsal strategies over time and sensitivity to serial position effects
  • Minimized differences in rehearsal strategies with nonverbal distractor tasks between immediate and delayed retention intervals
  • Serial position effects minimized by filler items at beginning and end of list
• LTL displayed poorest recall – consistent with previous studies showing left-hemisphere dominance for verbal memory across emotional and nonemotional domains
  • But when LTL compared with RTL, no differences between word type and retention interval. Both were equally insensitive to influence of arousal on memory
• Any lateralized effects for medial temporal lobe during emotional-processing tasks may be highly sensitive to stimulus modality or methodological variables.
• In a past study, temporal lobectomy patients showed retention advantage for nonarousing words that were positive or negative in emotional meaning when memory was assessed immediately after encoding. Emotional words form a more cohesive semantic category than neutral words. Such categorical processing may not rely on temporal lobe mediation
  • TL patients only show deficit for remembering emotionally arousing words over time
• Cahill et al. (1995) – Case study of patient with bilateral amygdala lesions due to Urbach-Wiethe disease. Deficit in recognition memory for emotional story, but since memory wasn’t assessed at more than one retention interval, unclear whether deficit was related to consolidation or other factors.
  • Emotional elements of a story focus attention on central features during encoding. This case study might highlight arousal-mediated attentional function of the amygdala.
• Alternative hypotheses
  • Deficit in TL patients related to damage in adjacent cortex. Cannot be ruled out until patients with more focal lesions are studied.
  • Deficit is due to hippocampal damage and not amygdala damage.
    • Authors don’t believe this hypothesis is tenable because the animal literature implicates amygdala and because another study showed intact memory enhancement for emotional pictures in amnesic patients with spared amygdala functions

Original source:

LaBar, K.S. & Phelps, E.A. (1998). Arousal-mediated memory consolidation: Role of the medial temporal lobe in humans. Psychological Science, 9, 490-493.

The AP just reported a story that vividly illustrates the incredible capacity of the human brain and body to perform under intense pressure. A Kansas man named Nick Harris was driving his 8-year-old daughter to school last week when he saw a car back up and run over a neighbor’s 6-year-old daughter.  “I didn’t even think. I ran over there as fast as I could, grabbed the rear end of the car and lifted and pushed as hard as I could to get the tire off the child,” Harris said.

The story continues:

He realized the little girl was Ashlyn, a friend of his daughter’s. Harris carried the screaming first-grader to the sidewalk and was going to get his phone to call 911, but Ashlyn said she wanted him to stay with her. He told people nearby to get the child’s mother, who lives a block away. There were no witnesses to confirm what happened. But Ottawa police Lt. Adam Weingartner said, “I don’t have anything to dispute it.”

Hough said Ashlyn told her Harris lifted the car off her, Weingartner said. Weingartner, the first officer at the scene, said Harris “was amped up pretty good. The first words out of his mouth were, ‘I lifted the car off the girl.’” He said it appeared Ashlyn wasn’t pinned under the car long enough to be seriously hurt, Weingartner said. Hough said her daughter was released from the hospital that afternoon with a concussion and some scrapes.

It’s an amazing story, if not totally watertight: there were no witnesses, and what happened to the car that ran the girl over? But Harris’ feat, while incredible, is not impossible. Chapter Two of Extreme Fear begins with the story of a similar episode, in which a Tucson man ran to lift a car off a bicyclist trapped underneath.

Because most of us rarely find ourselves in life-or-death situations, it can be hard to appreciate what a powerful effect fear can have on our physical speed and strength. Under acute stress, the sympathetic nervous system prepares the body for sustained, vigorous action. As the adrenal gland dumps cortisol and adrenaline into the blood stream, blood pressure surges and the heart races, delivering oxygen and energy to the muscles. It’s the biological equivalent of opening the throttle.

Vladimir Zatsiorsky, a professor of kinesiology at Penn State who has extensively studied the biomechanics of weightlifting, draws the distinction between the force that our muscles are able to theoretically apply, which he calls “absolute strength,” and the maximum force that they can generate through the conscious exertion of will, which he calls “maximal strength.” An ordinary person, he has found, can only summon about 65 percent of their absolute power in a training session, while a trained weightlifter can exceed 80 percent. Under conditions of competition a trained athlete can improve as much as 12 percent above that figure. Zatsiorsky calls this higher level of performance “competitive maximum strength.” This parameter is not a fixed number — the more intense the competition, the higher it can go, as the brain’s fear centers progressively remove any restraint against performance.

But there’s a limit to how fast and how strong intense pressure can make us. We’ve all heard stories about panicked mothers lifting cars off their trapped babies. They’ve been circulating so widely, for so long, that a great many assume that they must be true. Zatsiorsky’s work, however, suggests that while fear can indeed motivate us to approach more closely to our absolute power level than even the fiercest competition, there’s simply no way to exceed it. A 100-pound woman who can lift 100 pounds at the gym might, according to Zatsiorsky, be able to lift 135 pounds in a frenzy of maternal fear. But she’s not going to suddenly be able to lift a 3000-pound car.

What has our Kingdom come to when a man and members of his family are tied up by knife-wielding masked intruders and threatened with death, some of the victims escape, get help, chase the perpetrators and beat up badly one of them, only to be jailed for excessive use of force…?!?!?

This is effectively what has happened to Munir Hussain and his brother Toker who were jailed this week for 30 months and 39 months respectively. Walid Salem, the intruder they caught, suffered such injuries (including, it is claimed, a permanent brain injury) in what  was clearly a sustained attack by the Hussains that he was considered unfit to be tried on a charge of unlawful imprisonment and was merely put on a supervision order. In sentencing the Hussain brothers, Judge John Reddihough described the assault on Salem by the Hussain brothers as “a dreadful, violent attack”.

It undoubtedly was. Among the implements the Hussains and 2 other neighbours used to beat Salem were a cricket bat and a metal pole, (Reportedly the cricket bat was used to strike Salem with such force that it broke in 3!)

“This case is a tragedy for you and your families,” the judge told Munir Hussain. “Sadly, I have no doubt that my public duty requires me to impose immediate prison sentences of some length upon you. This is in order to reflect the serious consequences of your violent acts and intent and to make it absolutely clear that, whatever the circumstances, persons cannot take the law into their own hands, or carry out revenge attacks upon a person who has offended them.”

If the judge feels required by the law to pass such sentences, then the law is the proverbial ass!

Reddihough may know his law books but I suspect he’s not that familiar with human psychology.

The psychological scenario
Munir Hussain and his family returned from worship at their mosque during Ramadan. Devout Muslims, they will have been part-fasting for several days so the chemical balances – blood sugars, hormones, neurotransmitters, etc, will have been at different levels than is their norm – thus making it more likely that the Hussains would respond to trauma in an abnormal or exaggerated way.

Whether a court of law should be able to take into account the psycho-physiological effects of religious observance is a moot point. But undoubtedly the abrupt withdrawal of food over a short period of time will have affected the Hussains’ state of mind.

In their house, the Hussains found 3 masked intruders waiting for them. They were tied up, with their hands behind their backs, and forced to crawl from room to room. They were threatened with death. Shaheen Begum, Mr Husssain’s wife, told the court she feared the intruders had killed her youngest son. She said: “They were hitting my husband. When I asked them to stop or looked up they started hitting him again. They told us to lie face down and not speak, or they would kill us. It was very terrifying.”

It is rare for people in such terrifying circumstances to think coolly and rationally as Judge John Reddihough and his ‘law’ seem to expect. In most people the amygdala, the emotional centre of the brain, will become highly aroused, causing the hypothalamus to trigger the mechanisms which flood the body with the ‘fight or flight’ hormones adrenaline and noradrenaline. Munir Hussain was geared to action and reaction, not logical thought. Psychiatrist Dr Philip Joseph told the court Munir was normally a calm man who kept himself under control; but, on this occasion, in what defending QC Michael Wolkind called “the extreme moment of stress”, his body took the ‘fight rather than flight’ option.

This intense physiological arousal led in part to Munir Hussain freeing himself and, with the help of his brother, turning the tables on the intruders. That they then gave chase to intruder Walid Salem and assaulted him viciously is hardly surprising. It’s why soliders will carry on slaughtering the enemy when the enemy are helpless or desperately trying to surrender. They are far too caught up in the moment – amygdalas aroused – to think rationally. Many commentators – eg: Peter Foote & David Wilson (1970) have commentated on this ‘beserker rage’, originally lionised in Viking lore but still featuring in frequent accounts of battle, including those of recent US Congressional Medal of Honour winners.

Of course, what the Hussain brothers did in the end to Salem cannot be condoned. But it should be understood.

There is another factor in this tragedy; and that is the role of the RED vMEME. Doubtless, RED was behind much of the no-consequences actions of Salem and his confederates. However, there is also strong evidence this vMEME contributed to a strong and possibly overwhelming psychological impetus on Munir Hussain’s emotions and actions. According to The Times (15/12/09), Munir is reported to have felt that he was letting down his wife and children in not being able to defend them from the criminal attack of Salem and his accomplices. RED will not take such shame lying down; rather it will seek to put right the wrong of his shame in not being able to protect his family. Not only does the dominance of the RED vMEME in Munir’s selfplex at that moment in time need to  be recognised but so do the cultural memes which will have been influencing him. In Munir’s Asian/Islamic tradition – just as it was not that long ago in the European/Christian traditions – men are supposed to look after and protect their women and children. By not protecting them or being unable to protect them, they lose both self-respect and status in their community.

Walid Salem, also a Muslim and presumably familiar with the effects of Ramadan, chose to invade Munir Hussain’s house, tie up Munir and his family and subject them to death threats and other abuses. It can be argued that actions of Salem and his confederates precipitated the extreme arousal of Munir Hussain’s amygdala and the stimulation of his RED vMEME. As he was in a period of religious observance, it would be reasonable to expect Munir Hussain’s selfplex to be dominated by the decidedly more deliberate BLUE vMEME. Due to the actions of Salem and his cronies, different vMEMES were at play.

Thus, while Munir Hussain’s assault on Salem cannot be condoned, it is understandable and to some degree predictable. Thus, it can be argued Walid Salem chose knowingly to put himself in harm’s way.

A different story
Many commentators are comparing the case to that of Tony Martin, the Norfolk farmer who, in 1999, shot dead a teenage hoodlum who had been breaking into his property and terrorising him repeatedly.

This comparison would seem to be not entirely fair. Martin’s ‘manslaughter’ of his tormentor, lying in wait with a pump action shotgun, was clearly premeditated whereas Munir Hussain’s assault on Walid Salem could be considered ‘hot pursuit’. According to early reporting of the trial in This is London (25/08/09), Salem was punched repeatedly in the face while one of his assailants demanded “Who sent you?”

It would seem that the attack on Munir and his family was not in any way random but was directed at them in a very personal way. Prosecuting QC John Prine told the court: “Whatever the motivation of the attack, it was something of a personal kind. It didn’t seem to have been done out of a desire to steal anything, rather that it was directed at the people who lived there.”

How additionally terrifying must that have been, knowing that it was you and your family specifically under attack and not knowing who was behind it! (It would appear Munir Hussain has made a powerful enemy somewhere but no evidence has come to light of him being involved in any shady dealings – business or personal. Indeed, he is regarded as a proverbial pillar of the local community and has been offered the personal support of Chief Inspector Colin Seaton of the Thames Valley Police.)

Returning to Tony Martin, it’s worth noting that his original conviction for murder was reduced to manslaughter on the grounds of suffering from Paranoid Personality Disorder – hardly surprising given the persistent abuse he had suffered! As Battered Wives Syndrome is a permissible defence for women who cold-bloodedly kill their husbands perhaps years after abusive crimes against their person, Martin’s appeal on the grounds of being in an abnormal mental state could hardly be refused.

But how can Munir Hussain’s case be compared when his assault was immediate upon a ‘very terrifying’ ordeal whereas Martin’s was cold-blooded after months of abuse? While a psychiatrist would need to confirm this, I would hazard that Munir Hussain’s assault on Salem was driven by the RED vMEME’s desire to eradicate his shame while in a state of high physiological arousal due to the life-threatening ordeal he and his family had been subjected to and the fear that they were being targeted deliberately and personally to be harmed.

The failure of the criminal justice system
Judge John Reddihough’s words appear rather mealy-mouthed when he says: “…if persons were permitted to … inflict their own instant and violent punishment on an apprehended offender rather than letting justice take its course, then the rule of law and our system of criminal justice, which are the hallmarks of a civilised society, would collapse.”

…er, excuse me: Salem gets 2 years of supervision in the community while Munir is sentenced to serve 30 months behind bars…?!?!? 

It’s fine to outlaw taking the law into your own hands if the police could be guaranteed to arrive within less than 5 minutes of an alarm being raised (thus eradicating the need for ‘hot pursuit’ by the victims) – they can’t! – and if the criminal justice system were seen to punish the criminals and compensate the victims. Unfortunately too many victims of crime are aware of police indifference to all but the most serious of crimes while the criminal justice system is in a state of near-continual reform because the last set of reforms didn’t work either!

What would today’s criminal justice system have to say if Salem and his accomplices had gone ahead with their threats and murdered Munir Hussain and his family? I doubt their shades would have been much impressed with 20 years less 10 for good behaviour. (That’s assuming, of course, that the police could have caught the murderers…!)

The kind of inverse logic of Reddihough’s court is one of the problems with cultural dominance by the GREEN vMEME which, in its drive for egalitarianism, would put the rights of the criminals on a par with the rights of the victims.

Not only is this anathema to PURPLE’s need for safety in the community and BLUE’s desire for simple black & white justice – Salem chose to commit a crime, Salem should be punished – but it goes against the 2nd Tier ‘big picture’ of what is beneficial to society.

Salem is a habitual crook, with 50 previous convictions against him, currently awaiting trial on a charge of credit card fraud. According to Razi Shah, one of Munir’s lawyers, this last crime was committed after Salem had received such supposedly debilitating injuries –  “On the one hand he was claiming that he was suffering from memory loss and brain damage and is not fit to stand trial, and on the other hand he was out committing more criminal offences — and obviously complex ones such as credit card fraud.” (Interview with National Post, 15/12/09.)

Munir Hussain is a former chairman of the Wycombe Race Equality Council; his company employs 9 other people in worthwhile esteem-enhancing occupations and generates around £2.4M taxable revenue. Now, because of Reddihough’s decision, 9 (presumably-)respectable citizens lose their jobs and may be reduced to claiming benefit while the Treasury loses the taxes to be collected from £2.4M…?!?!?

Just what kind of insane society are we living in where the just are convicted on a technicality of law and the lawbreakers get off with unmanageable supervision orders..? (How many probation officers and social workers do we have spare to follow up on this kind of nonsense…? Clearly not enough since Salem went on to commit further crime!)

Of course, Munir Hussain can’t be allowed to walk free with his head held high. But the degree of his crime should be assessed in proportion to the provocation to which he was subjected, the degree of fear he was experiencing and the consequent state of mind he was in.

As for Reddihough’s awarding of criminal convictions, let’s just hope that Salem and the legal leeches who support him don’t decide to bankrupt the Hussain brothers with claims for compensation!

Insanity mustn’t rule!
For the benefit of law-abiding citizens, the law of self-defence needs broadening. If someone chooses to put themselves in harm’s way by breaking into your house and threatening you with death, then they clearly are the stimulus for the consequences that follow.

Of course, the Hussain brothers went too far; but it was Salem’s choice to put himself in harm’s way. Of course, the Hussain brothers need to be told they did wrong; but, if Munir’s amygdala hadn’t got so aroused that he fought his way free and, with his brother’s help, turned the tables on the intruders, he and his family might now be dead.

It’s absurd for people to be refrained in defending themselves in clear and obvious life-threatening situations because they’re worried they’ll go too far. They need that amygdallic panic energy to get themselves out of the situation…and, if the criminals come off badly out of that situation, well, the criminals shouldn’t have created the situation in the first place!

Of course, householders can’t be given a charter to do whatever they like to intruders – otherwise we really would end up with the occasional burglar being maimed, tortured and/or murdered in a quite callous and cold-blooded way.

But it’s not unreasonable to allow someone to defend their family and their home…and, if your amgydala is so aroused, you go too far…. Well, the French have long recognised the concept of ‘crime passionnel’ and many American courts have waived judgment on the grounds of ‘temporary insanity’.

That, to me, would be a fair judgment on the Hussain brothers: they were in a temporarily insane state due to extreme, life-threatening provocation, terrifying abuse and fear of an unknown enemy. And, as their victim deliberately caused that provocation and was party to that abuse, he should have no recourse in either criminal or civil law.

It’s in the public interest that the Hussain brothers should have a conviction for criminal assault. It sends out a clear message: push these guys way, way too far and you might get a beserker response. (Probably some 80% of the male population would respond similarly and, if their immediate family was threatened, around 50% of females.) Who but the stupid and the criminal would want to push them that far, anyway? Treat them with respect and dignity in a fair and equitable way and you will most likely find them fine citizens and good people to do business with.

What’s not in the public interest is to send to prison a wealth-generating pillar of local society for gross but single overreaction to extreme provocation and ongoing fear – that sentence destroying his business and the livelihoods of his workers. What’s not in the public interest is to set free a habitual criminal who then goes on to commit other crimes. What’s not in the public interest is to send a message to householders throughout our Kingdom that they must pause and think coolly when confronted with extreme danger to themselves and their families.

It’s to be hoped that the court of appeal has a bigger picture view of the law that Judge John Reddihough who appears to have been dominated by his BLUE vMEME’s absolutist views on rigid application of the law. The Hussain brothers should have their sentences suspended on condition of good behaviour. As for Walid Salem, perhaps the court will subject his claims to brain injury to a much more rigid scrutiny when considering his prosecution for credit card fraud. The police should also seek medical authority to haul Salem in and carry out a proper investigation into the attack on Munir Hussain’s home.

One of the main counterintuitive takeaways of the book is the idea that fear, though generally considered a negative emotion, can both feel good and be good for you. Now comes a study published in the American Journal of Psychiatry that points to the harm that can result from an inadequate fear response: The researchers found a link between fearlessness and future criminality in children as young as three years old.

The team, led by University of Pennsylvania psychologist Adrian Raine, revisited a group of subjects in Mauritius who had been tested for their reaction to loud noises as young children.  In the experiment, the children listened to two noises. One was followed by an uncomfortably loud blare; the other wasn’t. The New Scientist describes the outcome:

The children learned to anticipate which sound preceded the blare, and sweated in response to it – an indicator of fear. Decades later, Raine’s own team looked to see if any of the subjects had criminal records and found 137 that did. The team discovered that, as toddlers, these people had sweated significantly less in anticipation of the blare.

The result held true even after allowances were made for race,  gender, and socioeconomic conditions. The implication is that people who are unable to generate a sufficient fear response will not be able to correctly respond to threats in their environment — including punishment for aberrant behavior. The result is not wholly surprising. Damage to the amygdala has previously been linked to sociopathic behavior. And studies of pre-adolescent boys have found a correlation between fearlessness and the risk of later alcoholism.

All this raises a conundrum. Should we be testing our toddlers for this kind of deficiency as a way to identify those at risk of criminality? If so, should treatment for the excessively fearless be mandatory? At the far extreme, we can imagine a “Minority Report” type situation in which those with a supposed predilection toward law-breaking will be identified in childhood and either treated, incarcerated, or both. As the father of a one-year-old son, I think I’d prefer not to know about my boy’s predilections. I’d rather let myself believe that his future course will be a product of free will and fate.

October is the Autism Awareness Month in Canada.

April is the Autism Awareness Month in U.S.A. and in England.

April 2 is the Autism World Awareness Day. Here is the website of Autism World Awareness Day.

What is autism?

Contrary to common belief, autism is the “umbrella term” for a list of disorders as it is the same thing for epilepsy.

Autism spectrum disorder (ASD) is a range of complex neurodevelopment disorders, characterized by social impairments, communication difficulties, and restricted, repetitive, and stereotyped patterns of behavior. ASD occurs in 1 in 150 children (Amaral et al 2008).

Autistic disorder, sometimes called autism or classical ASD, is the most severe form of ASD, while other conditions along the spectrum include a milder form known as Asperger syndrome, the rare condition called Rett syndrome, and childhood disintegrative disorder and pervasive developmental disorder not otherwise specified (usually referred to as PDD-NOS). Although ASD varies significantly in character and severity, it occurs in all ethnic and socioeconomic groups and affects every age group. Experts estimate that three to six children out of every 1,000 will have ASD. Males are four times more likely to have ASD than females.

Brain structures affected with most consistent findings

Structural MRI findings have been inconsistent to an extent, however, recently more solid information has been gathered on the brain structures which play role in the mechanism of autism. The brain is enlarged in autism (Mosconi et al 2006).

Postmortem and structural magnetic resonance imaging (see the structural MRI entry for more information) studies have highlighted the frontal lobes, amygdala and cerebellum as pathological in autism. However, there is no clear and consistent pathology that has emerged for autism. Moreover, recent studies emphasize that the time course of brain development rather than the final product is most disturbed in autism (Gordon 2007). It is believed that the patients with autism are not born with the changes in the brain, these changes appear through the development of the child in the first year of life (Mosconi et al 2006).

Cerebellum

Although cerebellum has been implicated as taking role in several neurological and psychiatric disorders such as in schizophrenia, temporal lobe epilepsy, bipolar disorder (see Cerebellum: Dark side of the moon entry for more information on cerebellum), the changes in cerebellum (e.g., cerebellar size) have reported more consistently and cerebellum is relatively more important in autism. It has been suggested that increase in the volume of the cerebellum might indicate abnormalities in the cerebellar–cerebral circuits that most probably result in the learning difficulties (Gordon 2007). Not only volumetric studies, but also functional studies also imply a developmental problem in the cerebellum in autism (Gowen & Miall 2007). In neuropathological studies (in post-mortem brains) decreases in cerebellar Purkinje cells and other changes have been reported in patients with autism (Palmen et al 2004).

Amygdala

Amygdala (see the entry on amygdala for more information about the structure) was reported as enlarged in children with autism. It has been suggested that amygdala enlargement was associated with more severe anxiety and worse social and communication skills (c.ref. Amaral et al 2008) such as a relation between nonverbal social impairment and amygdala volume was reported by Nacewicz et al (2006).

Frontal lobe

Both functional and anatomical abnormalities are seen in patients with ASD. These change in the frontal lobe are related to changes in cognitive performance such as reduction in the cognitive processing speed (Schmitz et al 2007).

Some other brain structures

Although cerebellum, amygdala and frontal lobe are the structures with most consistent findings in autism, other brain structures have also been found to be affected in autistic patients (Baron-Cohen 2004). Volume deficit found in parietal lobe of autistic patients was correlated with narrowed spatial focus of attention (c.ref. Baron-Cohen 2004). Hippocampus is another limbic system structure changes of which has been reported in autistic patients (Palmen et al 2004).

Decreases in the corpus callosum size; the white matter between the two hemispheres of the brain conveying information between these two hemispheres. Relations between several cognitive performance tests and size of corpus callosum were reported in patients with autism (Keary et al 2009). The changes in corpus callosum supports the fact that there might be a decrease in the connection between the two hemispheres (Hardan et al 2009).

Caudate nucleus; is a part of the basal ganglia. The structures of basal ganglia play a role in task we do where we do not need to remember to do them, like riding a bike or typing. We do them automatically once we learn how to do them. Parallel to the function of caudate nucleus, a relation between caudate nucleus and repetitive behaviors was reported in autistic patients (Rojas et al 2006; see the second reference in the suggested readings to reach the free full-text on-line). Enlarged caudate nucleus was found in high-functioning medication-free autistic patients which is a valuable finding, as the medication used for the treatment of autism affects the size of the caudate nuclei (plural for nucleus; Langen et al 2007).

Brainstem (related to sensorial information pathology in autism), thalamus, and anterior cingulate cortex, superior temporal gyrus are among the other brain structures of which changes were reported in autism.

Functional studies

Functional studies such as functional MRI , electrophysiological studies give us more information about the deficits in the brain networks. All these psychiatric disorders are now believed to be disorders with problems in the functioning of networks. A network is made by the several brain structures specific for a given task. A structure might belong to more than one network. Functional studies show problems in the functioning of some networks in autism. One of them is fronto-parietal systems/network specific for spatial (3-D) attention task. The pathways between cerebellum and cerebrum (the rest of the brain) contribute to this network. Although the role of cerebellum in attention in autistic patients has been questioned (Gowen & Miall 2007).

Suggested readings:

Understanding autism and related disorders: what has imaging taught us?

Regional gray matter volumetric changes in autism associated with social and repetitive behavior symptoms.

A boy with Asperger’s syndrome prepares a video on his thoughts about his disease with his mom.

Remarkable news on the memory-erasure front. A team led by Elizabeth Phelps at New York University has published a report in Nature this week about a technique for wiping out unpleasant associations by taking advantage of a psychological process known as reconsolidation. A good deal of research has gone on lately into the erasure of unpleasant memories, with the goal of treating people suffering from anxiety and PTSD, but so far the focus has been on using drugs, as I’ve described earlier.

This kind of emotional memory is processed in the amygdala, a crucial hub for coordinating the brain’s response to danger. Fear memories can be problematic because, unlike the conscious, “explicit” memories that are formed via the hippocampus — things like the name of a friend, or the number of pints in a gallon — they do not fade with time in the same way. As I write in Chapter 10 of Extreme Fear:

The amygdala’s memory system retains frightening associations permanently. If you’ve been bitten by white dog, your amygdala will never forget. But the memory can get overlaid by a positive or neutral association. If you later buy a friendly white dog, say, and spend day after day associating your pet with harmless fun, in time your fear of white dogs will be overlaid by a suppressing response generated by the medial prefrontal cortex. Your amygdala isn’t forgetting that white dogs are dangerous, but you’ve laid a new memory on top of it, like a linoleum floor over a trap door. The old unconscious fear connection remains, encoded subconsciously in the amygdala. Under stress, the buried fear can spontaneously reemerge.

In her study, Phelps explored the effect on extinction of  reconsolidation, an intriguing effect in which a memory that has been recalled into consciousness becomes temporarily malleable and subject to change. Previous experimenters have administered drugs, such as the beta-blocker propranalol, during the reconsolidation phase, and found that this can help erase painful memories. Phelps’ experiment was designed to see whether a similar effect could be obtained without the use of drugs. And the surprising answer was yes.

As described on the ever-insightful BPS Research Digest blog, Phelps sat her subjects in front of a computer screen and showed them blue and yellow squares. Day One was “acquisition phase,” during which the colored squares were paired with painful electrical shocks. (Or not, in the case of the experiment’s control subjects.)

Now that the bad memories were firmly in place, the experiment moved on to phase two: extinction training. On the second day, subjects were shown the colored squares in the exact same setting, but this time the image of the squares was not paired with the application of painful shocks. The real-life equivalent would be seeing a white dog after having been bitten by one. Gradually, you learn not to be afraid, but the emotional memory remains, subconsciously, able to return.

This is what the experiment found on day three, when the subjects were once again put in front of the screen and shown the colored squares. Even though they’d successfully completed the extinction training the day before, they nevertheless showed phsyiological evidence of a heightened fear response, such as sweaty palms. Though it had been damped down, the fear remained.

Here’s where the ground-breaking part of the study comes in. On day two, just prior to the extinction training, a subset of the subjects were shown an image of the colored squares on the computer screen. Then they went off to watch television for ten minutes, before coming back and taking part in the extinction training. The idea was that this brief reminder would be enough to activate the process of reconsolidation — to make the fear memory plastic, so to speak, so that extinction could not only over-write the fearful memory, but actually erase it. And it seems that this is exactly what happened. On day three, those subjects who’d had the reminder ten minutes before extinction training showed no signs of fear at the colored squares. What’s more, the effect persisted when the subjects were called back into the lab a year later.

As with the propranalol studies, these findings point the way to more effective treatment of patients suffering from traumatic memories. What’s more, they suggest a technique that all of us can use to deal with fear in our daily lives, by increasing the effectiveness of home-brew extinction training. If you’ve had a phobia-inducing bad experience while speaking in front of a class, for instance, you can help extinguish that fear by practicing your presentation in front of a small group of friends. And to make the session even more effective, initiate reconsolidation by looking at the classroom lectern beforehand — or even just imagining it.

Oh, the agony! Nah, not really. Just today, I received an email from an agent I pitched to, regarding a full MS. Not quite, she says, although your premise is saleable. I don’t know whether to be over the moon that something I wrote is considered saleable or crushed by the feeling of rejection. Spurned. Thrown back onto the heap. One must then delve deep into the dark, murky waters of…self-esteem…and the dreaded emotional concotion that goes down to your first memory, buried there in the amygdala. Do I really want to go that far? Hell, no! Lets just leave it to my Taurean practicality and my pyramidal number 3 with its far-reaching practicality to strangle the incipient writer’s depression at birth. I’m on my 6th MS. I don’t have time for self-pity.

confined by time
we are liberated by the power
of the moment.

break the ice
on the surface of the water trough.
the goat
is thirsty this morning
and the horses in the barn
don’t want to share.

this snow pea weather
snaps my amygdala
across time

i am wide eyed

staring up through ice
at grey beard me

This footage was taken from inside the cockpit of an F-16 fighter jet piloted by Air National Guard Captain Chris H. Rose. In June, 1996, he was flying back to his base from a training mission when his engine failed with a loud bang. Here’s what happened next:

At the time of the accident, Rose was at an altitude of 13,000 feet, and above a layer of thick clouds. Immediately he turned in the direction of the nearest airstrip, at the Elizabeth City Coast Guard base. But where was it? With the help of his fellow pilots in the squadron he found his way through the clouds and broke out into clear air at 7,000 feet. From there, it was just a question of keeping his wits while nursing his damaged aircraft onto the runway.

What’s particularly interesting to me is the sound of Rose’s breathing, clearly audible on the tape’s audio track.  While it sounds heavy — clearly the breathing of a man under stress — it’s not excessively fast. He was not on the verge of hyperventilation. If he had been, he might well have lost control and panicked.

The connection between breathing and self-control has been recognized for centuries, but only recently has a scientific connection between the two been identified. Last week, the journal Cell published a paper in which researchers at the University of Iowa described how protein channels in the cell walls of neurons in the amygdala were found to be sensitive to varying levels of carbon dioxide in the blood. The amygdala is the region within the limbic system of the brain that plays a central role in coordinating the fear response. By blocking this channel, researchers were able to mute the fear response of rats.

This discovery helps explain how panic attacks can seem to strike out of the blue. In a time of stress, a person might subconsciously breathe too quickly, leading to excess levels of carbon dioxide in the blood. The amygdala, responding automatically to these increased levels, triggers a suite of physiological responses, such as  sweating, increased heart rate — and faster breathing. A vicious cycle takes hold, as hyperventilation leads to ever-higher levels of carbon dioxide.  All of a sudden the victim of the attack finds herself in the grip of an intense physical reaction without any idea why.

If this model is correct, then there’s a potentially very positive upshot. A drug that can block the protein channel might help prevent panic attacks and other related anxiety disorders. Who knows — it might even come in handy for pilots who lose their engines at 13,000 feet.

Last week, an old climbing buddy, Eileen Bistrisky, invited me to a presentation by Canadian climber, Don Bowie. K2 – The Ascent of the Savage MountainI was both inspired and horrified as he described his successful ascent of K2 without the use of supplemental oxygen.. At 28,253ft above sea level, K2, located in Northern Pakistan is the world’s second highest peak. It is widely considered to be the hardest and most dangerous mountain on earth to climb. On July 4th, 2007, Don became the 4th Canadian to summit.

Those are the raw stats. But they don’t begin to describe the strength of character of this young man. Not only did Don and his two team mates make it to the top, shortly after watching a fellow climber slide by and disappear over the edge of a cliff forever. But on the way down, in the falling dark, he stopped to help a fellow climber who had collapsed and was lying motionless in the snow. He could have kept walking. In fact, one got the feeling from hearing the story that the large majority of climbers on that mountain, would have done just that.

While helping that guy down to camp four, Don lost his footing and shot down the icy slope. Maybe it was karma, but it seems it was not his time to die, as he slid feet first into a snow-bank and stopped. 10 feet either was and he would have been toast.

The good news was that he was still alive. The bad news was that his toes on one foot were facing the wrong way; down instead of up – He had badly fractured his ankle. However, when you only have one good leg and you are 24,000 feet up a mountain, you might as well  be dead.

Unbelievably, other than his team-mates, no one else offered him any assistance. Don was stunned. Finally, just before the treacherous ice falls, getting impatient with the lack of empathy, he lashed out in frustration. This seemed to have guilted a few of the otherwise oblivious climbers into action and with that, they carried him through the last stretch. As it turns out. Don, did make it to base camp in one piece and with the help a US Army helicopter, he made it the rest of the way home.

In the ensuing Q and A, someone asked why he was willing to help a fallen comrade when he was surely close to total exhaustion himself. (remember, he has been climbing without oxygen) This is where Don really blew me away…

He said, “I train so that when I’m down to my last 5%, and I’m at the end of my rope, that my default mode is kindness”.

Kindness, now that’s an interesting concept. How many of us are even aware that when push comes to shove, when our brain is being hijacked by pain and fatigue that we even have a default mode? And how many of us have been conscious enough, in that storm of emotions, to be able to step back and pay attention to how we feel, how we are behaving and how we are being perceived? Now, take it one step further…How many of us train to control our behaviour in default mode?

I’m going to suggest that that level of self awareness is pretty rare.

Neurobiologically, we are driven into fight or flight mode when our amygdala, the part of the brain that perceives danger, flips the switch triggering the sympathetic nervous system which responding to the amygdala’s wailing siren, prepares us to either put up our dukes, or get the hell out of Dodge.

On the other hand, when we are down to our last 5%, lactic acid coming from our fatiguing muscles sends an inhibitory signal to our sensory cortex that says, “Batten the hatches, we’re going down”. At that point, parasympathetic functions like consciousness, digestion, cognition and the like start shutting down to conserve energy.

That is why you have to train your default mode.

Because, whatever happens at that point had better be automatic or else it’s not going to happen. So, in fact, not only do you have to have an idea of what you want your default mode to be, but you have to practice putting yourself in that situation over and over in order to train yourself to behave the way you want to in default mode.

In my daily work as an addictionologist, I work with people who are precisely those who in their QuestForFire become completely unconscious of the consequence of their actions Their default mode is to use drugs and alcohol as a way of coping with their dysphoria. I’m not saying that in a pejorative way. It’s just the way it is. That’s the definition of addiction. Continued use of drugs or alcohol as a way of managing distress despite evidence of continuing negative consequences.

So that is why I was so impressed with Don Bowie. In his QuestForFire, his mindset is exactly the polar opposite of impulsivity. In fact, it is the essence of impulse control.

And, when you look at the massive social, economic and interpersonal harm that results when we are unable to adequately control our impulses, you can see the amazing value of Don’s ability to ride the horse, instead of letting the horse ride him.

I for one struggle with my impulse control. It may be in my genes as I come from a long line of short-tempered Spaniards who are known to succumb to temptation. I’m not trying to make excuses. It’s just that I often find myself doing and saying things in default mode that make me shake my head.

“What were you thinking”? I wonder to myself. That’s just it. I wasn’t thinking. I was in default mode. So now the challenge is to imagine a more sensible default mode and to see if I can behave differently enough times to crack the mould and hopefully sculpt something I can be proud of.

Next week we’ll talk more about impulse control, what’s behind it neurobiologically and how we can harness it.

Cheers, A

Dr. Anthony Ocana   MD, MSc, CCFP, ABAM                                                               Family Physician, Addiction Specialist                                                     drocana@telus.net

The Los Angeles Times (http://tinyurl.com/amygdala-and-crime 11/17, Kaplan) “Booster Shots” blog said that, according to a study published online Nov. 16 in the American Journal of Psychiatry, “criminal behavior may be hard-wired — to some degree — in children as young as three and could be the result of a malfunctioning amygdala.” During the 1970s, researchers “recruited 1,795 three-year-olds” and “gave them a” tone-based “test designed to measure whether their amygdalas…were developing normally.” Twenty years later, “137 of the subjects…had criminal records.” Re-examining “their childhood tests, the scientists found that their reactions to the pleasant and high-pitched tones were the same,” results that were “in stark contrast to the other subjects, who learned to fear the high-pitched tones.”

Here’s a gene whose relationship to mental function is very straightforward.  If you hold your breath, your blood pH falls (more CO2 leads to more free H+ protons dissolved in your blood stream).  You also may become anxious, or worse if you are forced to hold your breath.  How does this process work?

Ziemann et al., in their new paper, “The Amygdala Is a Chemosensor that Detects Carbon Dioxide and Acidosis to Elicit Fear Behavior” [doi 10.1016/j.cell.2009.10.029] show that the acid sensing ion channel-1a (ASIC1a) gene is a proton-sensing Na+ and Ca++ channel – designed to activate dendritic spines when sensing H+ and drive neuronal activity.  Mice that lack this gene are not sensitive to higher CO2 levels, but when the protein is replaced in the amygdala, the mice show fearful behavior in response to higher CO2 levels.  Mother nature has provided a very straightforward way – ASIC1a activation of our fear center – of letting us know that no oxygen is a BAD thing!

Project H.M.

H.M. is considered to be one of the most famous cases in neuropsychology. His dense amnesia contributed significantly to our understanding of human memory. On December 2nd, exactly a year after his death, anyone interested will have the chance to watch the dissection of his brain. I’m really looking forward to this (that sounds a bit weird).

According to the Project H.M. official blog:

“On December 2nd, 2009 we will begin slicing the brain of the amnesic patient H.M. into giant histological sections. The brain specimen is going to be frozen and sectioned whole during one continuous session that we expect will last approximately 30 hours”

If you’re interested in finding more about the project and the next phase, visit the Project H.M. website

Clive Wearin’s Diaries @ Wellcome Trust Exhibition

A few months ago I wrote a post on Clive Wearing, another case of amnesia. If you’re lucky enough to live in London, you’d be interested to know that the Wellcome Trust’s new collection, titled “Identity: Eight Rooms, Nine Lives” hosts Wearing’s famous diaries in the Samuel Pepy’s room. The exhibition will be on from today until April and it’s a part of The Identity Project (Pressure Drop could also be interesting). Oh, and it’s free.  For more information visit the exhibition’s website. They have a special section on Clive Wearing including a number of interesting videos.

image: Salvador Dali’s – the disintegration of the persistence of memory

Israelilaisten tutkimustulosten mukaan kannabiksen käyttö voi auttaa post-traumaattisesta stressistä kärsiviä potilaita.

Haifan yliopiston psykologian osaston oppimisen ja muistin laboratorion tutkijaopiskelijan Eti Ganon-Elazarin toteuttama tutkimus selvitti kannabiksen vaikuttavuutta lääketieteellisenä hoitona traumaperäisestä stressihäiriöstä kärsiville potilaille. Traumaperäinen stressihäiriö esiintyy pienellä osalla traumaattisen tapahtuman, kuten auto-onnettomuuden tai terroristihyökkäyksen, kokeneista ihmisistä. Häiriössä esiintyy kuukausia – joskus jopa vuosia – tapahtuman jälkeen kestäviä henkisen paineen tiloja. Oireet käsittävät painajaisunia, takaumia, ylivalppautta ja minkä tahansa traumaan viittaavan välttelyä.

Journal of Neuroscience -tiedejulkaisussa esitelty tutkimus perustui synteettisen kannabiksen annosteluun rotille, jotka osoittivat samankaltaisia fysiologisia vasteita stressille kuin ihmiset. “Aivoissa on kannabinoidireseptoreiksi kutsuttuja reseptoreita kannabikselle”, kertoi tutkimusta valvonut tohtori Irit Akirav Haifan yliopistosta. “Me aktivoimme näitä reseptoreita amygdalaksi kutsutulla tietyllä aivojen alueella, joka liittyy stressiin, tunnemuistiin ja traumaattisten tilanteiden reaktioihin.”

“Stressillä on tiettyjä vaikutuksia tunneperäiseen oppimiseen”, Akirav selitti. “Stressi esimerkiksi haittaa ekstinktio-oppimista, joka on kyky oppia, että jokin on turvallista. Traumaperäisestä stressihäiriöstä kärsivillä ihmisillä on vaikeuksia ekstinktio-oppimisessa. Me yksinkertaistettuna osoitimme, että aktivoimalla tiettyjen aivoalueiden kannabinoidireseptoreja tämänkaltaiset stressireaktiot voidaan estää tai kumota, mikä sallii tästä häiriöstä kärsivien oppivan jonkin asian olevan turvallinen.”

“Tutkimus ehdottaa synteettisen kannabiksen käytön olevan mahdollista traumaperäisestä stressihäiriöstä kärsivillä potilailla”, tohtori Akirav päätteli. “Seuraavana vuorossa ovat pilottitutkimukset ihmisillä.” Akiravin laboratorion tohtorikokelas Eti Ganon-Elazar suoritti tutkimuksen. “Ajatellaan että joku on ollut läsnä linja-autoon kohdistuneessa terroristihyökkäyksessä”, sanoi Ganon-Elazar, “Tällöin linja-autosta tulee traumaattisen tapahtuman symboli ja henkilö saattaa vältellä linja-autoja tämän jälkeen.”

“Useimmat tuon kaltaisen traumaattisen tapahtuman kokeneet toipuvat ja kykenevät lopulta käyttämään linja-autoja”, hän sanoi. “Mutta joillakin on jo olemassa olevia ongelmia, he ovat esimerkiksi joutuneet useampaan traumaattiseen tilanteeseen elämänsä aikana. Näiden ihmisten on usein erittäin vaikea enää koskaan nousta linja-auton kyytiin, koska heidän elimistönsä on erityisen haavoittuvainen. Yleisenä ideana meillä oli, että kannabiksen käyttö voi auttaa tämän kaltaisia ihmisiä oppimaan, että on turvallista käyttää jälleen linja-autoa.”

Ganon-Elazarin tutkimus toteutettiin kolmessa osassa. “Ensiksi altistimme joukon rottia traumaattiselle tilanteelle, tässä tapauksessa erittäin lievälle sähköiskulle pimeässä huoneessa”, hän selitti. “Rotat eivät pidä valosta ja  yleensä ne pysyttelevät pimeissä tiloissa, mutta sähköisku sai rotat välttelemään pimeään huoneeseen tulemista. Jonkin ajan kuluttua rotat kuitenkin menivät pimeään huoneeseen, eikä niille annettu sähköiskua, joten ne oppivat että tila ei ole enää vaarallinen.”

“Otimme kuitenkin joitakin rottia ja altistimme ne lisästressille laittamalla ne korkealle tasolle kokonaan toisessa huoneessa”, Ganon-Elazar sanoi. “Rotat pelkäävät tilanteita joita ne eivät voi kontrolloida. Huomasimme, että tällaista lisästressiä kokeneet rotat oppivat huomattavasti vaikeammin, että pimeä huone on turvallinen. Näillä rotilla oli oppimisvaikeus, joka esti niitä menemästä pimeään tilaan.”

“Sitten otimme kolmannen ryhmä rottia, jotka altistettiin sekä sähköiskulle että korkean tason aiheuttamalle stressille, ja annoimme niille annoksen kannabiksen ainesosia jäljittelevää synteettistä ainetta”, Ganon-Elazar selitti. “Vaikka ne altistuivat lisästressille, tämä kolmas ryhmä palasi pimeän tilaan muutaman päivän jälkeen aivan kuten ensimmäinen ryhmä, joka ei kokenut ylimääräistä stressiä.”

“Tästä päättelimme, että synteettisen kannabiksen käyttäminen voi itse asiassa kumota henkiselle paineelle altistumisen aiheuttamaa huonontavaa vaikutusta kyvyllemme oppia, että jokin asia on turvallista.” Traumaperäinen stressihäiriö on suhteellisen yleinen Israelissa, erityisesti terroristihyökkäysten kohteeksi joutuneilla, holokaustista selvinneillä ja Israelin sotien veteraaneilla. Israelin hallitus ei ole hyväksynyt traumaperäisestä stressihäiriöstä kärsivien kannabiksen käyttöä, se odottaa vielä kliinisten kokeiden tuloksia.

Lähde:

http://www.themedialine.org/news/news_detail.asp?NewsID=27014

I was born with blessings and some curses.  I suppose that is not unusual, that’s what a lot of people would say, but let me fill you in on mine.

My blessings were a brain that has an IQ of over 150, and a big strong male body with a tolerance for pain.  My curses were I was born somewhat autistic (Asperger’s is the closest on the spectrum) and I had severely crossed eyes, indicative of central nervous system issues during gestation.

I probably would have been OK with the Asperger’s alone because of my intelligence, even with all the other issues I have had long periods of “success” in the workplace, but clearly people would have still thought I was a bit goofy.  Well of course if you are goofy and successful then they call you “eccentric.”

But when I was five, between kindergarten and 1st grade, my family made the decision to correct my eyesight with eye surgery.  I don’t blame my parents for this decision, they had to make it and I think they did the best they could, there is no doubt in my mind that they loved me deeply.

What happened is one day my mom gave me a book to read like “Tommy Goes to the Hospital”  It was really a picture book with a few words that mom and dad read to me.  Then one day mom gave me a little red pill to take, I took it and laid down to take a nap.  When I awoke I was in the hospital.  It was scary, and I didn’t know why I was there.

Very early the next morning the nurses gave me another red pill and then an hour or so later they strapped me into a gurney and wheeled me to the operating room.  I was awake, and my memories are of a couple of doctors and a couple of nurses in scrubs with masks on, and the very bright light straight above me.  I was strapped down, I couldn’t move.  After that they put a mask over my face and gave me some ether as a general anesthetic.  I will never forget that sickly sweet smell!  I think it knocked me out for a few minutes but I awoke to experience torture –  I was awake while someone (another human being) was sticking a sharp knife in my eye.  This was torture that I experienced, and it has had profound effects on my entire life.  I am not bitter at the doctors, in one way the surgery was successful and I have had a lifetime of relatively good eyesight.  The problem is that they knew I was conscious, I was screaming!  I could not escape.  The doctors I guess had to make decisions too.  They may have figured that a young child would not remember bad things like that, or they may have calculated that more anesthetic would risk killing me.  I am not telling you this to fix blame on them, you just need to know what happened, and you need to know that young children DO remember trauma.

I had recurring memories of  the hospital stay and the surgery (complete with ether smell) throughout my childhood, though curiously the memories themselves did not bother me much.

When I reached the age of 18 and went off to college, I was sitting in a math class one day (a class I really enjoyed, no math anxiety here) when out of nowhere BOOM I started sweating, shaking, I had trouble breathing, I had to jump up in the middle of the lecture and run out of the room.  After about 10 minutes things returned to normal.  I had had the first panic attack in my life. A week or two later, in the same classroom, I had a second panic attack, even more severe than the first.  I really thought I was having a heart attack!  It too subsided but the next day I went to student health services and they checked me out, said I didn’t have any heart problems, I was a healthy 18 year old, and that all that had happened was that I had got some “nerves.”

Back in 1968 very little was known about PTSD so I don’t fault the people at the clinic.  There were at that time literally thousands of WWII and Korean War vets on the sidewalks in Skid Row Los Angeles.  Back then they were called “bums.”  Just like people call the homeless “bums” now.  Some things never change.  Now we know that these vets were suffering from what was called “combat fatigue” but what we call PTSD now, and they were self-medicating with alcohol and other drugs.  Even to this day there is a stigma attached to PTSD with some people at least, because it is clear that some people go through the same or similar bad experiences and don’t get PTSD.  The deniers of PTSD simply say that those who acquire PTSD are “weak.”

What are the consequences of having PTSD?  First, panic attacks, which I believe are brought about by a constant high level of adrenaline in the body.  I think that what happens at the moment of trauma is that your body is overwhelming swamped with adrenaline, fight or flight, but that you become traumatized because you are in a situation (restraint, wounded, incapacitated) where you can neither fight or flight.  When that happens, the adrenaline remains in your system for too long and literally burns up some neural pathways.  In many situations, the act of fighting or fleeing provides exercise to your body and the adrenaline is burned off rapidly.  Where the damage occurs is in the amygdala  and associated regions in the central part of the brain, that ancient part that is often referred to as the “reptile brain.”  The damage to the brain is organic and probably irreversible, certainly not by surgery and it is impossible for me to see how a drug therapy can repair physically damaged neural pathways deep in the brain.  Recent advances in medical imaging technology have confirmed that there are indeed physical differences in the brains of the traumatized and untraumatized.

And I think once you have had a panic attack, you are more likely to have more, you are likely to become predisposed.  This is because a panic attack is a horrible experience.  You literally feel like you are having a heart attack, like you are going to die on the spot.  You become worried that you will have another panic attack, and you become “hyper vigilant”, a part of your brain starts constantly monitoring your bodily functions like heart rate, perspiration and breathing.  A little up tick, caused by something minor like a rude check out person at the supermarket or someone butting in line ahead of you, or someone cutting you off in traffic, can put you right into full panic if you are hyper vigilant.  Why?  Because there is no rational reason for your body to feel that way, so it must be another incipient panic attack.   There are cues in the environment that are triggering your panic, but until you get more aware of how panic works you will simply assume that you must have a physical problem (like a heart attack.)

Another consequence of PTSD is anger.  This is usually directed inward towards yourself and outward at the same time.  I think that it is directed inward because somehow you feel that you could have done more to avoid the situation where you were traumatized.  Anger directed inward seems to lead to depression, complicating your life even further. Anger is directed outward at society as a whole, because in your mind it is unbelievable what some fellow human beings did to you.  Needless to say, anger directed outward can have some bad consequences.  But I don’t think most people with PTSD anger are dangerous.  Several times I have encountered a vet walking down the street yelling and screaming at all the world.  Sometimes I have engaged them in conversation, and all the ones who would talk to me had a decent coherent conversation with me for five or ten minutes, they told me their story, and then they went off down the street yelling and screaming.

Just in the last four years or so I discovered within myself a direct link between panic attacks and anger.  I discovered that if I let myself get really angry, then a panic attack was almost surely to follow in its heels.  Since I made that connection, I strive not to be angry.  It is not always possible, but sometimes walking away is good for your health.

It is curious that many children who are traumatized at an early age do not show any symptoms until they reach adulthood.  In my case I started getting serious panic attacks at 18-19 years of age, and they continue to this day, though in the last few years they have lessened.  The only symptoms I had as a child were an incredible fear of doctors, hospitals, medical devices, needles, etc.  Also around age 16 I developed serious insomnia, which left me haggard almost every day.  It took me hours most nights to get to sleep, and that continued up til about 6 years ago, when a therapist hypnotized me.  Of course in my mid-life I used whiskey to go to sleep, that was the only way I could have enough rest to get up and work in the morning.  It was a short term solution and seriously bad for my health.  I did also have vivid  recurring memories *visual, smell, taste, pain) of the torture all through my childhood but they didn’t seem to bother me.  After I started getting the panic attacks, I stopped for the most part having those memories return.

I think the reason that traumatized children are shielded from some of the worst effects of trauma have to do with the biology of  human evolution.  We are standing on the apex of several million years of hominid evolution, and for 98 percent of that time, most humans never reached the age of 30.  It was important for the survival of the species that juveniles reach mating age, without the problems that PTSD would cause them, but it was less important that adults have that genetic protection.  Children and juveniles were raised in common by the tribe or clan, all the children had lots of “parents” so adult shielding from trauma was simply not needed for survival in the evolutionary sense.  Evolution is economical.

Insomnia is debilitating, and many PTSD victims suffer from it.  They have nighmares.  They have worrisome recurrent dreams with unsolvable problems.  They are hyper vigilant, so when they lay down to sleep every little tinge in the body that is unusual is cause for concern.  Many of them turn to alcohol – like I did – in order to get to sleep at all.  Of course sooner or later you get the rebound – the alcohol wears off in a few hours and you find yourself wide awake at 3 AM.  In my case I also had hypnagogic jerks.  This is the sensation you get when you are almost asleep, but you get “jerked” back awake, like someone has startled you.  Another factor is that when I was 16 I witnessed my father have a stroke and dying while he was sleeping.  It was not pretty, he had lost all bodily function and control, with his eyes wide open but blank.  By all measure (maybe his heart was still beating) he was dead before the ambulance left.  For years after that (until a few years ago I was terrified that I would die in my sleep.   I felt this terror every night.  By the time I was 30, I needed to have the lights on in order to go to sleep, I had to have the TV or radio on to go to sleep, and I had to have some whiskey in me to go to sleep.  There were two things in my life that complicated my sleep problems at that time.  First of all I was a heavy tobacco smoker.  Tobacco constricts the blood vessels, and when I lay down to sleep my heart was always pounding like a hammer.  Since I was hyper vigilant you can understand where that took my thoughts.

Another complication was my work schedule.  At around 30 I got a job as a supervisor in a casino, one of the youngest in that position in Reno.  The problem was it was a relief shift.  That means I had to work 2 graveyard shifts 1 AM – 9 AM, Two day shifts (9 AM – 5 PM) and one swing shift (5 PM – 1 AM) EVERY WEEK.  Although it was a good job opportunity I have to say in retrospect that working that schedule for 3 years was very destructive of my health, both then and in years to come.  For someone who already had serious sleep problems, I am lucky it didn’t kill me.  I would never do it again, I wouldn’t ask anyone to do it, and I think work schedules like that should be illegal.

I worked steadily all through my 30’s and did not have many panic attacks.  I was self-medicating with alcohol (but not at work, I was a conscientious employee.  I did need a few shots at the end of the work day to get right.

At the age of 42 my life fell apart, I used to say it was like a bomb went off in my life.  Separation and divorce, child custody fight, bankruptcy, several relocations, the beginning of real health problems like dental disease, loss of our home to foreclosure, and the loss of my career in the casinos.  Any one of those qualifies as one of the most stressful events in life, and I had five or six of them in one year.

I spent the next 8 years working in minimum wage jobs, some of them heavily physical, which at my age completed the breakdown of my body.  About that time I came the closest I have ever come in life to killing someone.  I got hired on at a pallet plant – a place where they scavenged broken pallets from around the area and then tore them apart and rebuilt them.  Hours of work there was 6 AM until 4 PM with one half hour lunch and two 10 minute breaks.  The work was outside in the sun (I was working in August) and there was no shade.  They handed me a nail gun and pointed to a stack of pallets and told me to get to work.  The pallet yard was next to an elementary school and since I had no idea what I was doing, about 5 or 6 times a day I would hit the board wrong and a nail would go whanging off into the distance.  I could hear it ping in the school yard when it landed.  There were two brothers who ran the operation and they were both abusive drunks, one of them was worse than the other.  (A few years later one of them went to jail for attempting to murder his sibling.)   One day they asked me to sort some boards into piles, but they assumed that I would know the criteria of how they wanted them sorted.  I did the best I could, but around noon the little bastard came up to me, using the foulest language called me the stupidest person he had ever met.  I was tired and cranky and I had a 2 x 4 in my hands.  My impulse was to simply split his skull with it, and I was a big strong boy then.  Thankfully I didn’t kill him, but I looked him in the eye and layed the stick down.  Somehow I think he knew what I was thinking.  I finished the shift but never went back.

All during this period I was aware that I had some mental issues.  I knew I had panic attacks and anxiety.  Sometimes I was extremely depressed for a couple of months.  I experienced agoraphobia at times.  I developed OCD.  I searched constantly for a psychotherapist to help me.   I found a few in that period but most of them were not very good.  One good one I had dropped me when I lost my job (and my insurance) when the casino I was working in folded.  One problem I have had with psychotherapists is that I am much smarter than most of them.  A few were bright, but with those I would rather have an intelligent theoretical conversation than do therapy.  It is a problem for a therapist when your patient is constantly critiquing your methods and even the basis of your mode of therapy.  Most of them don’t enjoy it.  I know that now.

By my late 40′ s I realized that I was drinking too much – that I was likely an alcoholic. I know, some of you will say I should have figured it out 10 years earlier, but it was alcohol that allowed me to function in any way near to normal, and it didn’t cause me major problems in my life.  (I didn’t have any DUIs, I didn’t get into bar fights, I didn’t beat the wife and children.)  I did quit for a couple of months in 1996.  But I was suffering then from extreme agoraphobia (I could barely leave my apartment) and I got referred to a program run by the University.   That’s when I met the SSRI family.   I had two months when the only time I left my apartment was the once a week journey 8 blocks to the group therapy session that was supposed to help me.  Well it was a cluster fuck.  I was extremely agoraphobic, but I was being forced to be in a room of a dozen or so strangers, most of whom were in their 20s and they were there for amphetamine or heroin abuse, or for domestic violence.   We had absolutely no commonality.  After a month of that I started drinking again in order to be able to go to the meeting!

The psychiatrist who was in charge of the program gave me Zoloft to help with my panic and agoraphobia.  It didn’t work.  As a matter of fact, when I was taking the Zoloft it was the first time in my life that I felt “crazy.”  Up to that point I knew I had problems but I had never felt like that.  I found myself walking down the sidewalk, and all of a sudden I would find myself “stuck”.  I could not move either forward or back.  Sometimes I would just stand there for up to 10 minutes before the stuck feeling went away.  After 10 weeks or so of the Zoloft I convinced her that it wasn’t working and she switched me to Paxil.  She started me off with (I found out later) double the normal therapeutic dose.  I took Paxil for the next 17 weeks and it was the absolute worst period of my life.  My agoraphobia deepened.  I kept all my curtains closed because I was afraid that the sun would come up.  (Meaning that when the sun comes up you should go out and function.)  A couple times a day I could crack my door open and peek out.  I had plenty of food because at that time I was an OCD hoarder – I had stocked up!  I was no longer going to group therapy because the group had ended.  The presumption is that 8 weeks or so of therapy is enough.  Around this time, since my panic was worsening she gave me a bottle of 100 ativans.  Now lots of people like benzos, I don’t, for me they were similar to drinking alcohol but without the happy.  I went through the ativans in a month and she gave me a bottle of klonopins, another benzo.  I was still taking the Paxil and I wasn’t drinking.  My agoraphobia deepened further and my panic became almost constant, from the time I awoke in the morning until I went to be at night.  Some times I would awaken to a full on panic attack.  For the first time in my life I developed tremors, in both arms and both legs.  At one point I could recognize seven distinct varieties of tremor in my body, and I even had some idea of the types of thought that triggered each one.  I could not stop them.

After 2 months of klonopin and paxil I had a heart to heart talk with her over the phone.  I had reached the point where I was in constant panic, so the way I used the klonopin was to take one and see if I could sleep.  I would wait a half hour or so and take another one.  Sometimes I had to take 4 in order to sleep.  They didn’t help at all with my panic, I panicked right through the klonopin.  Of course the way I was taking the klonopin was dangerous, and she knew it and I knew it.  I was honest with her.  She asked me how many klonopins I had left and I told her I didn’t have any.  She told me that the klonopins weren’t working so I needed to stop.  So I cold turkeyed off 5 klonopins a day because I didn’t have any and I had no access to any.  That was about 3 days of pure hell, far worse than quitting alcohol cold turkey.  I don’t know what she was thinking about, but she shouldn’t have a medical license.  What she put me through was dangerous.  When coming off these drugs, you must taper down.

It was around that time that I had the first suicidal impulse in my life.  I had walked over to the shrinks to get the prescription for my second months of klonopin and I was on my way to the pharmacy which was located on the other side of the railroad tracks.  As luck would have it, a freight train was coming down the tracks.  I had a sudden impulse to step in front of it.  The impulse was pretty strong but I didn’t do it.  I never felt that way again until about late 2005.  But the thing about suicidal thinking, once it happens to you I think you are prone to get it again.

In that year also I had my first experience with AA.  I had quit drinking, but the people who were “helping” me put pressure on me to go to AA.  So I went and it was a disaster.  I am not an AA basher.  What happened is the night I chose to attend the meeting they had a “candlelight” meeting.  I found myself still in high agoraphobia, sitting in a dark candle lit room with 40 strangers.  There was a constant movement of people in the dark around me as those 15 or 20 who were there under court order went up and got their attendance verified.  I made it to the end of the meeting, when all of a sudden everyone stood up and clasped hands.   I was trapped inside the circle.  I had to leave in a hurry thankfully I didn’t run anyone down on the way out.  I had to walk past several bars on the way home and somehow I managed to stay out of them too.

About 2 weeks after I cold turkeyed off the klonopin I called her again as I was running out of Paxil.  I told her my condition (constant panic and extreme agoraphobia)  and she decided to take me off the paxil.  She asked me how many I had left and I told her that I had one tablet left.  She told me to break it in half and take a half each day.  That’s how she tapered me off paxil!  I had an extremely rough five or six days.  One thing you have to experience is the “snaps” that is the snap, crackle, pop that you hear INSIDE YOUR HEAD when you are coming off paxil.   For 5 or 6 days I had the strangest dreams I had ever had in my life, though not all of them were scary.  The sensations I experienced in coming off Paxil were similar to the sensations you get when you are coming on to LSD.  One night I had a vivid dream of Satan.  One night I had a vivid dream of the gorgon Medusa from Greek myth.  I had a dream of my own birth, sliding down the birth canal and taking my first breath.  I have never had dreams like these before or since in my life.

There is a reference to panic and PTSD in Greek Mythology, and that is the story of Perseus and Medusa.  Anyone who approached the gorgon Medusa and looked at it was immediately frozen into place.  This is similar to the effect of a visual cue for a panic attack.  You look at it and suddenly you are frozen by fear.  Perseus solved this problem by looking at Medusa in a mirror, looking at the fear in an indirect way, and thus was able to slay the monster.  Out of the blood of Medusa sprung winged Pegasus.  I have taken cues from this myth in my own program of rehabilitation, trying to find indirect means to attack the panic.  The early Greeks at the dawn of civilization were a warrior race, and most certainly were aware of the effects of trauma in their fellows.  I think that this was expressed in myth.

Once the paxil was out of my system the constant tremors went away, but I have been bothered with them ever since intermittently, especially when I am facing some stress.  However I did lapse into a severe depression, about 6 weeks, the deepest depression of my life.  I could not get out of bed.  I did realize after a few weeks that I had to do something or I would simply die.  I went and got some whiskey and found myself a job.  I still didn’t drink on the job, but by now I sure needed that bottle by 5 or clock or so.  I was working doing heavy duty lifting in a warehouse at age 48 and alcohol was my only medicine for my agoraphobia and the constant pain of neuropathy and dental pain.

All through this period my dental health was deteriorating as well.  In 95 I was working at a casino and I bought the insurance plan.  I even paid extra for “dental coverage.”  I went to the dentist (I had to go with my therapist to keep me calm) and he said he could do the work required for five or six hundred dollars.  It turned out that the dental coverage I had been paying for covered only one exam per year, but no real dental procedures.  I was barely surviving at that time I had no extra income above my basic requirements of food and rent.  A year or so later I got sent to another dentist by the vocational rehab program in town.  When I told the dentist that I got panic attacks, he told me that he couldn’t treat me because “he didn’t want to get attacked.”  What a moron.  I could tell you lots more about dentists but I am starting to get angry.

In November 2000, my health collapsed.  I was working full time, but one morning I simply couldn’t get out of bed.  I called in sick.  I had liver disease, my skin was yellow and my belly and legs were swollen.  My sister took me to the hospital and the nurse asked me how long I had had liver disease.  It was a puzzler for me, because I didn’t know I had liver disease.  I  think I may have died that day, briefly.  I know I saw the light when I passed out in the exam room.  I have not had a sip of alcohol since.

By early 2001 I had landed in a half way house in Reno.  I weighed 230 lbs. when I entered the hospital, and in six weeks my weight went to 155.  I had lost 75 lbs. in six weeks.  My arms looked like pipestems.  I spent 19 months at the halfway house.  I will say this, they kept me alive.  Some people are under the impression that these county half way houses are run at the expense of the local taxpayer.  What happens really is that the social worker signs you up for presumptive SSI, maybe $800 a month or so from the federal government.  The county takes all of that money every month, we were given an allowance to spend of $82 a month.  So it is really the federal government and the residents who are paying for their stay.  If you are on SSI, you are not allowed to seek employment (that is how it was then) but you did have to apply for permanent disability in order to continue staying there.  I applied for SSD as they asked me to and I was sent to a doctor for a review.  The doctor examined me and asked me “Why do  you think you are incapable of working?”  I answered him that I thought I was capable of working.  I was probably wrong, but I had worked all my life and I still had the ethic.  My application got turned down and again I was forced to appeal it.  I had to hire a lawyer $4000 contingency and when the judge decided I was disabled I had also repay the county $7000 that it said I owed them for my time at the halfway house.  So basically I paid the county $25000 for 19 months of two meals a day and sharing a bedroom with a stranger.

A few years later I had my experience with Effexor.  The therapist I was seeing worked with a doctor and she prescribed me Effexor.  Given my experience with Paxil I was not eager to take it but I did.   I took it for 6 weeks or so and I found myself becoming more and more aggressive.  I was living in one of those low income apartments where you share a kitchen with three other units.  Well if you have a miracle that works out but most of the time one or two of your kitchen mates are addicts, thieves, or paranoid schizos.   I got sideways with one of my neighbors a guy as big as me but a few years younger.  I found myself walking up to him in the lunch room and calling him out to his face, I took off my shirt and roostered around the complex, I became very aggressive.  I am ashamed of this now, I have never acted like that in my life, and since I quit the Effexor I haven’t acted that way since then.  It is not in my nature.

I realized that the Effexor was causing me to act that way.  It was making me aggressive.  I called up the doctor and told her that the Effexor wasn’t working.  She said she would work something out and I should call the pharmacy in a couple of hours.  It turned out when I called the pharmacy that she had decided to tritrate my dosage UP.  The other thing is that up until then she had given me free samples.  I was poor.  I had less than 10 dollars to my name.  The cost of a months Effexor for me at the new double dose would be almost $250.  That was a friday night, and I was about to have a very bad weekend cold turkeying off Effexor.  Maybe it was a lack of communication, but I clearly told her that the Effexor was making me feel violent.  I literally wanted to beat my neighbor to death with my bare hands.  I knew that I couldn’t take the Effexor any more and at any rate I couldn’t afford to fill the prescription.  Effexor is a double medication, it contains an SSRI component and an older anti depressant component.  Bottom line is that quitting Effexor cold turkey is like walking off a cliff.  That weekend I experienced the worst panic attack of my life and a quick sharp descent into the unspeakable darkness.  Among other things I did that weekend is I gave away my car to a stranger walking down the sidewalk.

Yeah sure, taper off.  You can see how well that works in real life.

I know this has been a long depressing monologue, but somewhere around 2004 I started getting SSD, and I was able to stabilize my finances, rent a better apartment and do a bit better in general.  I started getting politically active, because I had come to see how corrupt and greedy our health care system is.  When it became clear that our government was torturing people, I started working to impeach George Bush and that gang of criminals around him.

I would say that the last 3 or 4 years of my life has been blessed.  I have not conquered all my fears or solved all my problems but I have more friends now than I have ever had.  I have music.  I live in a beautiful part of the world.  I stopped being angry at women and started simply enjoying their beauty and accepting from them what they could give me willingly.  I accepted that the chances of an autistic like me for a long term relationship with any woman are slim.

have a peaceful day,

Bill

Flickr: Courtesy of artsy_T

According to an article in the American Journal of Psychiatry, a 20 year study has found that children who are fearless as toddlers are more likely to commit crimes as adults.

The study was conducted to determine whether an impairment of the amygdala, part of the brain’s limbic system which works to generate a fear response, was linked to criminal behavior.

Nearly 1,800 three-year-old children in Africa were exposed to two different sounds, one pleasant and one unpleasant, and their fear response was measured based on sweat secretions created when the unpleasant sound was played.  Sweat is a physiological response to fear, and therefore the absence of sweat secretions associated with the playing of the unpleasant sound indicated poor fear conditioning.

Twenty years later researchers used court records to determine how many study participants had committed serious crimes, and found that all of the 137  individuals who had committed serious crimes demonstrated poor fear conditioning at 3 years of age.

The study suggests that its finding support a “neurodevelopmental theory of antisocial and criminal behavior.”

I can’t emphasize enough, however, that correlation does not prove causation.  As the study states, many other environmental factors, such as family size and parents’ education level, among others, also play a part.  In addition, it is likely that other important factors, such as psychosocial stressors, socioeconomic status, trauma history, parents’ criminal history, as well as participants’ education level affect fear conditioning and future criminal behavior.   Yu Gao, a research associate that helped conduct the study and was interviewed by U.S. News, admits, “There’s no 100 percent correspondence between conditioning deficits and crime. Not all poor conditioners will become criminals and not all criminals have the early fear conditional deficits.”  Thus, it is also important to remember that many children in the study who showed poor fear conditioning as children did not go on to commit crimes.   A follow up study to determine what factors were different for the children who showed poor fear conditioning but were able to avoid criminal behavior will be important.  In fact, the findings of such a study will likely be more valuable than those of the current study, as it can point toward prevention.  Also, a follow up study conducted on the same participants today to determine if there has been a change in fear response will likely be beneficial.

The article points to childhood enrichment programs as important for assisting in the proper development of the amygdala, as well as prenatal programs to assist in eliminating maternal drug and alcohol use.  It is likely that other factors- such as increase in supports, financial resources, parental behavior, education, and parental involvement also will play a part in prevention of future criminal behavior in children.

Future studies need to focus more on what specific factors enable children with poor fear conditioning to behave appropriately in society in later life.  The findings of these studies can then help to create new programs and resources for children and families.

To see an article about the study published by U.S. News, click the following link: http://health.usnews.com/articles/health/healthday/2009/11/17/fearless-3-year-olds-might-be-tomorrows-criminals.html

A recent GWAS study identified the 3′ region of the liver- (not brain) expressed PECR gene (rs7590720(G) and rs1344694(T)) on chromosome 2 as a risk factor for alcohol dependency.  These results, as reported by Treutlein et al., in “Genome-wide Association Study of Alcohol Dependence” were based on a population of 487 male inpatients and a follow-up re-test in a population of 1024 male inpatients and 996 control participants.

The authors also asked whether lab rats who – given the choice between water-based and ethanol-spiked beverages over the course of 1 year – showed differential gene expression in those rats that were alcohol preferrers vs. alcohol non-preferring rats.  Among a total of 542 genes that were found to be differentially expressed in the amygdala and caudate nucleus of alcohol vs. non-alcohol-preferring rat strains,  a mere 3 genes – that is the human orthologs of these 3 genes – did also show significant association with alcohol dependency in the human populations.  Here are the “rat genes” (ie. human homologs that show differential expression in rats and association with alcohol dependency in humans): rs1614972(C) in the alcohol dehydrogenase 1C (ADH1C) gene, rs13273672(C) in the GATA binding protein 4 (GATA4) gene, and rs11640875(A) in the cadherin 13 (CDH13) gene.

My 23andMe profile gives a mixed AG at rs7590720, and a mixed GT at rs1344694 while I show a mixed CT at rs1614972, CT at rs13273672 and AG at rs11640875.  Boooring! a middling heterozygote at all 5 alcohol prefer/dependency loci.   Were these the loci for chocolate prefer/dependency I would be a full risk-bearing homozygote.

The human brain is very good at forgetting, a fact that I was recently reminded of when my bank asked me to choose from a series of “security questions” as part of an account upgrade. What was the name of my third-grade teacher? What was the name of the street my school was on? What city was my mother born in? I was astonished at how little of this kind of thing remained in my memory bank.

Forgetting this kind of explicit memory comes easily, but there’s another kind of memory we’re not so good at erasing. Memories of fearful experiences seem to stay with us forever. To the extent that their impact fades over time, it’s not because we forget them, but that our brains gradually suppress them. They’re forgotten, but not gone. And they can cause problems for people suffering from emotional trauma, when buried memories come roaring back to inflict pain all over again.

It would be better if the brain were able to forget some kinds of fearful memories just it can things like names and phone numbers – and a recently published paper presents evidence that might just be possible. Researcher Nadine Gogolla and colleagues demonstrated that as the brain of a baby mouse matures, its ability to form permanent fear memories develops at the same time as a net-like structure forms in the amygdala, where emotions are processed and fear-related memories are stored. Made of proteins called chondroitin sulfate proteoglycans, this “neural net” structures seem to prevent memories from being erased. When they’re disrupted by a drug, mice are more likely to lose those memories.

The finding points the way to a possible therapy for human fears: a drug that would alter the formation or functioning of the “neural net” and thereby allow people to shed troubling and disturbing memories. It’s still a long way off, but the research indicates that it could at least be possible.

By Darren Schreiber

I’m testing out a potential new feature for the neuropolitics listserv entitled “Regions of Interest.” I’ll be giving a brief overview of a portion of the brain that is relevant to neuropolitics. I’ll include a few brain images that will help orient readers as to its location, a description, and a discussion of its relevance to the social cognition. I will then provide a set of citations to recent articles that discuss the region, with particular emphasis on interesting experiments, meta-analyses, and reviews.

I’m starting off with the amygdala. This region has become almost a household word in the past decade. The typical way it is discussed is in its role in the experience and processing of fear. However, the story is far more nuanced than that. This almond sized region is located in the limbic system, deep within the brain, as can be seen in the axial, coronal, and sagittal images shown above.

I would particularly draw your attention to the meta-analyes listed below (7 & 9) as a way of getting a broader sense of the amygdala’s role. While it is active during fear and other negative emotions, it is also active during positive emotions and a variety of forms of social cognition (2 & 4). A particularly interesting line of work demonstrates that while this region is susceptible to automatic or subliminal activation, it is also down regulated by conscious mental processes (7). Its role in the processing of race has gotten a lot of attention (3, 5, 13) as people appear to have higher amygdala activations when viewing African Americans. However, darker skin tones in general seem to trigger the amygdala (13). It has also been implicated in risk and reward processing during decision making (6 & 12). My colleagues and I have some preliminary work suggesting that Republicans can be identified by their stronger activity in this area during a risk task. Finally, I would draw your attention to the review by Joseph LeDoux (11). He and Ralph Adolphs have been leading researchers in the amygdala’s role in the brain, particularly its function in social cognition.

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1. Tsuchiya et al. Intact rapid detection of fearful faces in the absence of the amygdala. Nat Neurosci (2009) vol. 12 (10) pp. 1224-5The amygdala is thought to process fear-related stimuli rapidly and nonconsciously. We found that an individual with complete bilateral amygdala lesions, who cannot recognize fear from faces, nonetheless showed normal rapid detection and nonconscious processing of those same fearful faces. We conclude that the amygdala is not essential for early stages of fear processing but, instead, modulates recognition and social judgment.
2. Kennedy et al. Personal space regulation by the human amygdala. Nat Neurosci (2009) vol. 12 (10) pp. 1226-7The amygdala plays key roles in emotion and social cognition, but how this translates to face-to-face interactions involving real people remains unknown. We found that an individual with complete amygdala lesions lacked any sense of personal space. Furthermore, healthy individuals showed amygdala activation upon close personal proximity. The amygdala may be required to trigger the strong emotional reactions normally following personal space violations, thus regulating interpersonal distance in humans.
3. Platek and Krill. Self-face resemblance attenuates other-race face effect in the amygdala. Brain Res (2009) vol. 1284 pp. 156-60People respond favorably toward self-resembling faces. We investigated the pattern of responding in the amygdala of Caucasian participants to self-face resemblance expressed in same and other-race (African descent) faces. The amygdala response was 1) non-linear to faces as a function of self-facial resemblance and 2) attenuated to other-race self-resembling faces when regressed with implicit racial attitudes. These findings demonstrate that interactions of important facial social judgements are processed combinatorially in the amygdala.
4. Said et al. Nonlinear amygdala response to face trustworthiness: contributions of high and low spatial frequency information. J Cognitive Neurosci (2009) vol. 21 (3) pp. 519-28Previous neuroimaging research has shown amygdala sensitivity to the perceived trustworthiness of neutral faces, with greater responses to untrustworthy compared with trustworthy faces. This observation is consistent with the common view that the amygdala encodes fear and is preferentially responsive to negative stimuli. However, some studies have shown greater amygdala activation to positive compared with neutral stimuli. The first goal of this study was to more fully characterize the amygdala response to face trustworthiness by modeling its activation with both linear and nonlinear predictors. Using fMRI, we report a nonmonotonic response profile, such that the amygdala responds strongest to highly trustworthy and highly untrustworthy faces. This finding complicates future attempts to make inferences about mental states based on activation in the amygdala. The second goal of the study was to test for modulatory effects of image spatial frequency filtering on the amygdala response. We predicted greater amygdala sensitivity to face trustworthiness for low spatial frequency images compared with high spatial frequency images. Instead, we found that both frequency ranges provided sufficient information for the amygdala to differentiate faces on trustworthiness. This finding is consistent with behavioral results and suggests that trustworthiness information may reach the amygdala through pathways carrying both coarse and fine resolution visual signals.
5. Derntl et al. Amygdala activation during recognition of emotions in a foreign ethnic group is associated with duration of stay. Social neuroscience (2009) vol. 4 (4) pp. 294-307Cultural differences in emotion recognition performance have frequently been reported, whereby duration of stay in a foreign culture seems to be a crucial factor. Furthermore, cultural aspects influence the neural correlates of face and emotion processing thereby also affecting the response of the amygdala. Here, the exposure to a foreign culture and its influence on the cerebral correlates of facial emotion recognition were examined in 24 Asian and 24 age-matched European males. Subjects performed an explicit emotion recognition task and were imaged with a 3 T MR-scanner. Results demonstrate a significant cultural influence on the specific recognition of disgust and anger, with higher accuracy among the Europeans, while the functional data indicate generally elevated amygdala activation in Asians compared to Europeans. Moreover, a significant inverse correlation between duration of stay and amygdala response emerged, with stronger activation in those subjects with shorter duration of stay in Europe. The observed amygdala hyperactivation in Asians may reflect novelty aspects but might also be associated with greater effort and motivation in immigrants, thus it possibly reflects one neural correlate of the “alien-effect”. We conclude that exposure to a foreign culture and duration of stay affect the behavioral and neural response to facial expressions of emotions.
6. Seymour and Dolan. Emotion, decision making, and the amygdala. Neuron (2008) vol. 58 (5) pp. 662-71Emotion plays a critical role in many contemporary accounts of decision making, but exactly what underlies its influence and how this is mediated in the brain remain far from clear. Here, we review behavioral studies that suggest that Pavlovian processes can exert an important influence over choice and may account for many effects that have traditionally been attributed to emotion. We illustrate how recent experiments cast light on the underlying structure of Pavlovian control and argue that generally this influence makes good computational sense. Corresponding neuroscientific data from both animals and humans implicate a central role for the amygdala through interactions with other brain areas. This yields a neurobiological account of emotion in which it may operate, often covertly, to optimize rather than corrupt economic choice.
7. Costafreda et al. Predictors of amygdala activation during the processing of emotional stimuli: a meta-analysis of 385 PET and fMRI studies. Brain research reviews (2008) vol. 58 (1) pp. 57-70Although amygdala activity has been purported to be modulated by affective and non-affective factors, considerable controversy remains on its precise functional nature. We conducted a meta-analysis of 385 functional neuroimaging studies of emotional processing, examining the effects of experimental characteristics on the probability of detecting amygdala activity. All emotional stimuli were associated with higher probability of amygdala activity than neutral stimuli. Comparable effects were observed for most negative and positive emotions, however there was a higher probability of activation for fear and disgust relative to happiness. The level of attentional processing affected amygdala activity, as passive processing was associated with a higher probability of activation than active task instructions. Gustatory-olfactory and visual stimulus modalities increased the probability of activation relative to internal stimuli. Aversive learning increased the probability of amygdala activation as well. There was some evidence of hemispheric specialization with a relative left-lateralization for stimuli containing language and a relative right-lateralization for masked stimuli. Methodological variables, such as type of analysis and magnet strength, were also independent predictors of amygdala activation.
8. Adolphs. Fear, faces, and the human amygdala. Curr Opin Neurobiol (2008) vol. 18 (2) pp. 166-72The amygdala’s historical role in processing stimuli related to threat and fear is being modified to suggest a role that is broader and more abstract. Amygdala lesions impair the ability to seek out and make use of the eye region of faces, resulting in impaired fear perception. Other studies in rats and humans revive earlier proposals that the amygdala is important not only for fear perception as such, but also for detecting saliency and biological relevance. Debates about some features of this processing now suggest that while the amygdala can process fearful facial expressions in the absence of conscious perception, and while there is some degree of preattentive processing, this depends on the context and is not necessarily more rapid than cortical processing routes. A large current research effort extends the amygdala’s putative role to a number of psychiatric illnesses.
9. Sergerie et al. The role of the amygdala in emotional processing: a quantitative meta-analysis of functional neuroimaging studies. Neuroscience and biobehavioral reviews (2008) vol. 32 (4) pp. 811-30Functional neuroimaging studies have provided strong support for a critical role of the amygdala in emotional processing. However, several controversies remain in terms of whether different factors-such as sex, valence and stimulus type-have an effect on the magnitude and lateralization of amygdala responses. To address these issues, we conducted a meta-analysis of functional neuroimaging studies of visual emotional perception that reported amygdala activation. Critically, unlike previous neuroimaging meta-analyses, we took into account the magnitude (effect size) and reliability (variance) associated with each of the activations. Our results confirm that the amygdala responds to both positive and negative stimuli, with a preference for faces depicting emotional expressions. We did not find evidence for amygdala lateralization as a function of sex or valence. Instead, our findings provide strong support for a functional dissociation between left and right amygdala in terms of temporal dynamics. Taken together, results from this meta-analysis shed new light on several of the models proposed in the literature regarding the neural basis of emotional processing.
10. Murray. The amygdala, reward and emotion. Trends Cogn Sci (Regul Ed) (2007) vol. 11 (11) pp. 489-97Recent research provides new insights into amygdala contributions to positive emotion and reward. Studies of neuronal activity in the monkey amygdala and of autonomic responses mediated by the monkey amygdala show that, contrary to a widely held view, the amygdala is just as important for processing positive reward and reinforcement as it is for negative. In addition, neuropsychological studies reveal that the amygdala is essential for only a fraction of what might be considered ’stimulus-reward processing’, and that the neural substrates for emotion and reward are partially nonoverlapping. Finally, evidence suggests that two systems within the amygdala, operating in parallel, enable reward-predicting cues to influence behavior; one mediates a general, arousing effect of reward and the other links the sensory properties of reward to emotion.
11. LeDoux. Primer: The amygdala. Curr Biol (2007) vol. 17 (20) pp. R868-74The amygdala is a complex structure involved in a wide range of normal behavioral functions and psychiatric conditions. Not so long ago it was an obscure region of the brain that attracted relatively little scientific interest. Today it is one of the most heavily studied brain areas, and practically a household word. Art critics are explaining the impact of a painting by its direct impact on the amygdala; essential oils are said to alter mood by affecting the amygdala; and there is a website where you can unleash your creativity by clicking your amygdala, and thereby popping your frontal cortex. In this Primer, I will focus on the scientific implications of the research, discussing the anatomical structure, connectivity, cellular properties and behavioral functions of the amygdala.
12. Hampton et al. Contributions of the amygdala to reward expectancy and choice signals in human prefrontal cortex. Neuron (2007) vol. 55 (4) pp. 545-55The prefrontal cortex (PFC) receives substantial anatomical input from the amygdala, and these two structures have long been implicated in reward-related learning and decision making. Yet little is known about how these regions interact, especially in humans. We investigated the contribution of the amygdala to reward-related signals in PFC by scanning two rare subjects with focal bilateral amygdala lesions using fMRI. The subjects performed a reversal learning task in which they first had to learn which of two choices was the more rewarding, and then flexibly switch their choices when contingencies changed. Compared with healthy controls, both amygdala lesion subjects showed a profound change in ventromedial prefrontal cortex (vmPFC) activity associated with reward expectation and behavioral choice. These findings support a critical role for the human amygdala in establishing expected reward representations in PFC, which in turn may be used to guide behavioral choice.
13. Ronquillo et al. The effects of skin tone on race-related amygdala activity: an fMRI investigation. Soc Cogn Affect Neur (2007) vol. 2 (1) pp. 39-44Previous work has shown differential amygdala response to African-American faces by Caucasian individuals. Furthermore, behavioral studies have demonstrated the existence of skin tone bias, the tendency to prefer light skin to dark skin. In the present study, we used functional magnetic resonance imaging (fMRI) to investigate whether skin tone bias moderates differential race-related amygdala activity. Eleven White participants viewed photographs of unfamiliar Black and White faces with varied skin tone (light, dark). Replicating past research, greater amygdala activity was observed for Black faces than White faces. Furthermore, dark-skinned targets elicited more amygdala activity than light-skinned targets. However, these results were qualified by a significant interaction between race and skin tone, such that amygdala activity was observed at equivalent levels for light- and dark-skinned Black targets, but dark-skinned White targets elicited greater amygdala activity than light-skinned White targets.
14. Schaefer and Gray. A role for the human amygdala in higher cognition. Reviews in the neurosciences (2007) vol. 18 (5) pp. 355-63Considerable evidence suggests that the human amygdala plays an important role in higher cognitive functions in addition to its well-known role in emotional processing. In this article we review representative evidence showing the involvement of the human amygdala in long-term memory, working memory and attention. Results are discussed in terms of their relevance to current theories of amygdala function that can integrate its cognitive and emotional functions in a comprehensive framework.

Music is an important part of most people’s lives. Recently, many studies are focused on music and especially its relationship with emotion and the reward system. Here are a few interesting ones:

1.Salimpoor et al (2009), found that the rewarding aspects of music listening are related to the degree of emotional arousal. Here’s the abstract from their interesting study:

“Background: Listening to music is amongst the most rewarding experiences for humans. Music has no functional
resemblance to other rewarding stimuli, and has no demonstrated biological value, yet individuals continue listening to
music for pleasure. It has been suggested that the pleasurable aspects of music listening are related to a change in
emotional arousal, although this link has not been directly investigated. In this study, using methods of high temporal
sensitivity we investigated whether there is a systematic relationship between dynamic increases in pleasure states and
physiological indicators of emotional arousal, including changes in heart rate, respiration, electrodermal activity, body
temperature, and blood volume pulse.

Methodology: Twenty-six participants listened to self-selected intensely pleasurable music and ‘‘neutral’’ music that was
individually selected for them based on low pleasure ratings they provided on other participants’ music. The ‘‘chills’’
phenomenon was used to index intensely pleasurable responses to music. During music listening, continuous real-time
recordings of subjective pleasure states and simultaneous recordings of sympathetic nervous system activity, an objective
measure of emotional arousal, were obtained.

Principal Findings: Results revealed a strong positive correlation between ratings of pleasure and emotional arousal.
Importantly, a dissociation was revealed as individuals who did not experience pleasure also showed no significant increases
in emotional arousal.

Conclusions/Significance: These results have broader implications by demonstrating that strongly felt emotions could be
rewarding in themselves in the absence of a physically tangible reward or a specific functional goal.”

2. Activation in brain regions implicated in reward and emotion was also found in an earlier study by Blood & Zatorre (2001). Using PET they found cerebral blood flow increases and decreases in brain regions that are thought to be involved in reward/motivation, emotion, and arousal such as the ventral striatum, midbrain, amygdala, orbitofrontal cortex, and ventral medial prefrontal cortex. These structures are known from previous studies to be active in response to other euphoria-inducing stimuli, such as food, sex, and drugs of abuse.

3. Menon & Levitin (2005) also found that:

“listening to music strongly modulates activity in a network of mesolimbic structures involved in reward processing including the nucleus accumbens (NAc) and the ventral tegmental area (VTA), as well as the hypothalamus and insula, which are thought to be involved in regulating autonomic and physiological responses to rewarding and emotional stimuli.”

4. For more information on the neural correlates of music perception, you can read the reviews by Limb (2006) and Koelsch (2006).

(picture: part of Guilherme Marconi’s collection – My Schizophrenic Brain)

Links:

1. http://brainethics.wordpress.com/2009/07/17/fear-and-pleasure-in-the-amygdala/
2. http://en.wikipedia.org/wiki/Somatic_markers_hypothesis
3. http://tinyurl.com/yfh77c9
4. http://www.wnyc.org/shows/radiolab/episodes/2006/05/05
5. http://brainethics.wordpress.com/2009/08/04/damasio-on-emotion-fisher-on-love-peretz-on-music/

We are living creatures. Humans, animals…We have to survive in life. We communicate through people, as we do not live alone but in a society. For that, we use two aspects. Cognition and emotions. So here are the key words before we start “amygdala”.

Key words for amygdala

Survival

Communication

Emotion

Now..Let’s do the Five Ws and one H of the amygdala!

What is amygdala?

Amygdala means “almond” in Latin. See the two pictures below. The one on your right is an MRI image of amygdala on a coronal view (the way you would cut a bread; sorry for the analogy; I am so anatomist). Amygdala resembles an almond, doesn’t it? The Ancient scientists were creative.

 Where is amygdala?

The human skull is composed of different bones. One bone just over your ears, put your finger over your ear, here is your temporal bone. The lobes of the brain also lie in these bones with the same names. So your temporal lobe is under your finger now. Why did they name it “temporal”? Well, it comes from the term “time”. The connection is one starts to have grey hair starting from there as time goes by.

Here is a picture of Ben Stiller, one of my favorite actors, as I like romantic comedies. And here is more information for you. Open the temporal lobe and look inside, the medial temporal lobe (medial means close to the middle of something in the body, not close to the outside) as we anatomists call it. You will see 3 brain structures there. In the middle hippocampus, above it amygdala, under the hippocampus parahippocampus. And when someone says medial temporal lobe, basically you remember these structures and you remember that they are about remembering; e.g. memory. So the temporal lobe; grey hair; comes from “time” and medial part is about memory. Interesting, no? When it was named, it was not known that it was about memory.

When/Why do we use it?

A person is walking at the street approaching you. You just don’t like him and do not want to talk to him. Let’s say he is a politician, not your favorite. You are in the Middle East and getting ready to take off one of your shoes to throw at him. So here are the basic questions about your brain? How did you recognize him? Who is he? Amygdala is not in the scene yet. It is your hippocampus (next post) that gives you the facts. A list of information about him. Your reaction is a result of your emotional history; why are you reacting this way? Not because you remember his name, etc. But you should remember all these before you react. Amygdala is now in the scene with its role in “emotional processing”, “emotional learning” and “emotional memory”.

Let me take you again to the same street. Now it is after midnight; and not a safe place of the city to hang out after midnight. But you are there somehow. A “Oh-my God” looking not so well dressed guy stops you in the middle of the street where you are alone and asks for some change. You say “Sorry, I do not have any”, then the next thing you realize is a shining knife in dark. What do you do? You escape with all the blood in your legs, or you have a fight for your life. So what do you need? Fear. You should have the crisis plan. Hippocampus again tells you “this is a knife and can hurt or kill you”. Amygdala says “and you should freak out,now!”. Stress (too much is harmful though) is the key for survival for that night. Thanks God you have an intact amygdala for some emotional processing.

Emotional learning/Emotional memory/Emotional processing (particularly fear)

The amygdala as a key brain structure for acquisition and storage of fear memory traces. Emotionally significant experiences tend to be well remembered, and the amygdala has a pivotal role in this process. If you have an ordinary dinner with an ordinary friend, or have a dinner where you propose to your future wife, it is more likely that you remember the one with the ring in your pocket. Let me say that it is also important for your survival (so that the wife does not nag you when she asks you what she was wearing that night).

Functional neuroimaging studies have provided strong support for a critical role of the amygdala in emotional processing. Research on the neural systems underlying emotion in animal models over the past two decades has implicated the amygdala in fear and other emotional processes. Behavioral data suggest that fear stimuli automatically activate fear and capture attention. This effect is likely to be mediated by a subcortical brain network centered on the amygdala.

Smelling

Amygdala and the other structures of the medial temporal lobe where it is located is a member of the limbic system. The system was there in the brains of the first mammals. So amygdala is a part of the oldest region/system of the brain. What does it tell us? Something common with animals. Reproduction, sexual behavior, aggression, response to stress (fight or flight), emotions, survival. Amydala is important in smelling in our animal friends. Sexual arousal and survival (you smell the danger). This role and part of amygdala is not a big deal in humans, though.

Reward

Social perception

Higher cognitive functions (long-term memory, working memory, decision-making and attention)

Stress response:

This is good. But you can be in trouble on a plane when amygdala and the limbic system dominates in your brain if you are afraid of flying; sending “there is danger, panic, panic!” messages when there is none. Panic attacks? Yes, we have amygdala in the scene.

Psychologically induced stress with the blood pressure-regulatory system

Sexual behaviour

Who has abnormal amygdala?

Alzheimer’s disease

Anxiety disorders (such as generalized anxiety disorder, post-traumatic stress disorder, panic attacks; panic disorder)

Autism

Bipolar disorder

Epilepsy; temporal lobe epilepsy (my PhD dissertation topic)

Major depressive disorder

Schizophrenia

Substance abuse; drug addiction

How can we study amygdala?

Structural MRI studies where we have the volume of amygdala in several diseases (such as in major depression) have inconsistent results. There might be different reasons for that, but one reason might be amgydala is composed of different nuclei groups, oranges and apples together, these nuclei (plural of nucleus) function differently. Functional neuroimaging studies (functional MRI being again the most popular), animal studies are very useful as well.

Some links to amygdala or Miss. Amy G. Dala.

Anatomy of the brain: Amygdala

The Role of the Amygdala in Fear and Panic

Amygdala and its allies

Amygdala

The Whalen Lab

Neural pathways to long term memory: Hippocampus and amygdala

The king of amygdala anatomy and pathology: David Amaral from University of California, Davis

A recent book by J. LeDeoux; another king; Emotional Brain

A youtube video: Amygdala-the cause of all your anxiety.

A youtube video: Structural and functional neuroimaging of the amygdala

Duration- 53:06 min

A song by the Norwegian scando-pop duo Frost “Amygdala“

Emotional intelligence

http://amygdala.net/

“İnsanların çoğu kaybetmekten korktuğu için, sevmekten korkuyor. Sevilmekten korkuyor, kendisini sevilmeye layık görmediği için. Düşünmekten korkuyor, sorumluluk getireceği için. Konuşmaktan korkuyor, eleştirilmekten korktuğu için. Duygularını ifade etmekten korkuyor, reddedilmekten korktuğu için. Yaşlanmaktan korkuyor, gençliğin kıymetini bilmediği için. Unutulmaktan korkuyor, dünyaya iyi birşey vermediği için. Ve ölmekten korkuyor aslında yaşamayı bilmediği için…”

William Shakespeare’in “korku” hakkındaki bu sözleri beni korkunun kaynağına yani beyne yöneltti. Gelin birlikte bu kaynağı-fabrikayı yani beyni gezelim ve özellikle “korku”nun ve ondan açığa çıkan diğer duyguların bu fabrikada nasıl işlendiğine bir göz atalım…

Fabrika yani üreten kaynak “beyin” ve bu fabrikadaki binlerce işçi (nöron), kendine ulaşan bilgileri işlemekle, ortaya koymakla her an meşguldür. Ortaya koydukları işin vasıflarına göre sınıflanmış nöronlar, gruplar halinde kendilerindeki bilgi doğrultusunda gece ve gündüz, uyku hali ya da uyanıklık hali gibi durumlarla sınırlanmadan, yani bu durumlar onlar için bir şey ifade etmeden, “ölüm” denen tecrübeye kadar devamlı olarak çalışmaktadırlar. İşte bu nöron gruplarından biri olan ve özellikle korkuları, bu korkulardan doğan vehim, vesveseleri gibi pek çok duyguları oluşturan, “badem (amigdala-amygdala)” işçi grubu, beynin yani fabrikanın bir ucunda, limbik sistem denilen bölümde sağ ve sol iki küçük gruptan oluşmaktadır. Onlar için kısaca “duygusal beyin merkezi” denilebilir. Özellikle “korku”nun kaynağıdır, yaratıcısıdır. Limbik sistemdeki diğer grup olan “hipokampusla (hippocampus)” -ki bu grup anıların deposudur- koordineli bir biçimde çalışmaktadırlar. Hipokampus depolanmış bilgileri, anıları sinapslara yani elçilere, basit anlamda bioelektriksel olarak yükleyerek amigdalaya gönderir. Burada bu bilgiler “duygusal” nitelik taşıyan etiketlerle etiketlenerek, şablonlar halini alır ve tabii bu duygusal davranışların tepkimeleri yani ortaya çıkmaları da genellikle başta “korku” olarak nitelendirebileceğimiz davranışlar olarak fiile dökülür.

Eğer işin biraz daha derinine inersek…

Fabrikada değer yargıları ve şartlanmalarla programlanmış veri tabanı (data base) kaynaklı edinilen bilgiler ışığı altında amigdala, kendisine ulaşan her bilgiye “bu bana zarar verir mi?”, “bundan nefret eder miyim?” gibi sorularla vücuttaki hormonların yani belirli bir grup hücrenin çalışmasına sebep olur, bu üretilen bilginin hormonlar aracılığı ile “kardiyovasküler sistem”, “kaslar”, “bağırsaklar” adı altındaki diğer hücre gruplarını aktive ederken aynı anda da beyin köküne “daha hızlı nefes al, kan basıncı artsın!, hazım engellensin” gibi bilgileri geçerek çeşitli reaksiyonları oluşturur. Tabii bu gibi aktiviteleri yapmasının bir açıdan başlangıç diyebileceğimiz noktası, kendisine ulaşan bilgileri önceden kendisinde işlenmiş olan bilgilerle yani veri tabanındaki (data base) mevcut olan bilgilerle bir takım bağlantılar kurarak ve her bilgiye “duygusal” bir etiket yapıştırarak gerçekleştirmiş olmasıdır.

Bize “göre” “geçmiş” diye adlandırdığımız bir noktada yaşanmış “korku” etiketi altındaki bir bilgi, amigdalada mevcut olduğu için bir bakıma “ayna” fonksiyonu ile yani yansıtma, bir nevi “ tekrar görüntüleme” şeklinde o bilginin tekrar yaşanmasını ya da benzer bir deneyimin oluşmasına sebep olabilir. Örneğin, büyük bir gürültü duyduğunuzda, amigdala hemen bu gürültü ile ilgili daha önceki bilgiden ortaya çıkmış duyguları aktive ederek, aynı duyguların benzer olayda tekrar yaşanmasını sağlar; eskiden oluşmuş duygular, o yeni bilgiye- duruma aynı şekilde kopyalanıp, adapte edilir.

Görsel ya da duyuşsal durum dışında, bizim dışımızdaki(!) kişilerin yaşadığı duygusal durumlarda da aynı duygunun bizde de açığa çıkması, yansıması kaçınılmazdır. Prof. Dr Marcola Iacoboni bu durumu “ayna nöron”larla açıklamaktadır. Ona göre, karşımızdaki bir kişinin yaşadığı duygusal bir durum, ayna nöronlar vasıtası ile bizim beynimizdeki amigdalada daha önce yaşadığımız benzer duygusal durumlarla eşleşip, bizden de aynı şeklide açığa çıkabilmektedir.

Bu öylesine ilginç bir oluşumdur ki, amigdala herhangi bir “korku” ya da “endişe” etiketli kendisindeki ya da dışında diye algıladığı başka(!) birisindeki mevcut bilgiyi “duygusal” olarak etiketleyip, depolarken, bir yandan da buna benzer yeni bilgileri de oluşturduğu şablonlarla etiketleyip “süregiden bir korku-endişe-vesvese bilgisi zinciri” oluşturmaktadır.

Veri tabanımızdaki (data base) mevcut olan ve amigdalada “duygusal” olarak etiketlenen bilgiler ve bir de yeni bilgilerin de eski bilgilerle kıyaslanarak, işlenmesi bizleri tamamen “duygusal” bir girdaba sokmakta ve bu girdabın en kuvvetli elemanlarından olan “korku” ise tüm duygulara sanki hükmederek, zaman zaman akıl ve iradeyi devre dışı bırakmaktadır. Çünkü, beyinde yani bu fabrikada akılcıl olarak işlerin yürütülmesini sağlayan ve koordine eden “neokorteks (neocortex)”, limbik sisteme ulaşan bilgiyi amigdalanın tersine daha sağlıklı değerlendirip, yorumlayarak işlemden geçirerek limbik sisteme geri yollarken, amigdala kortekse göre daha hızlı işlem yapar ve kendisine gelen bilgiyi önceki bilgilerden birisine benzerlik gösterdiği anda uygunluğunu tespit edip, etiketleyip limbik sisteme geri yollaması ve ana işletim sistemde yerini almasını sağlar. Bu da bizim dışardan çoğu kere “duygusal” bazlı “fevri- önyargılı-vesveseli” davranış dediğimiz çıktılara yani fiillere sebep verir.

İşte bu gibi duyguların aklın önüne geçip, ortaya çıkması, bilincin hakikatine yönelik yaşamasını engelleyebilmektedir. Bundan dolayı, amigdalanın bu yöndeki duygusal etiketleme işleminin önüne geçmenin tek yolu, “iman” gücüdür. Bakın bu durumu Üstad Ahmed Hulûsi de 1996 yılında yazdığı“İslâm” adlı kitabının “Cehennemden Ne İle Çıkılır” bölümünde nasıl açıklamış:

“… insan, hayatını cehenneme çeviren vehim gücünün üstesinden akılla gelemez!. Vehim kuvveti yani “yoku var sanıp, varı yok sayma” özelliğinin üstesinden gelecek olan insandaki güç akıl değil, imandır!. Vehim, akıl ve ona dayalı olan tefekkür mekanizması üzerinde rahatlıkla tasarruf ederken, fiilleri direkt yoldan etkileyen iman karşısında daima yenik düşer!. İşte bu yüzdendir ki “Dini” anlaması için akıllıya teklif yapılmış ve iman ederek yürümesi önerilmiştir!.
İnsanın, gerek dünya yaşamındaki cehennemî sürec, ve gerekse de ölümötesi yaşamındaki cehennemi, hep onda galip gelen vehim kuvvesinin sonucudur!. Bunun sona erdirilmesi ise yalnızca iman kuvvesi ile mümkündür!…”

“

Sonuç olarak, beynimizde yani fabrikada çalışan iki küçük badem büyüklüğündeki grubun beynimiz üzerindeki duygusal etiketli (korku-endişe-vesvese gibi…) etkilerinin hakikati anlamaya ve yaşamaya doğru yol alan beyinler için farkedilmesi gereklidir. Bu farkedişle birlikte, atılacak adım, beynimizde mevcut olan sonsuz sayıdaki “Mutlak Bilinç”e ait özellikleri keşfederek, bu yönde, bu inanç doğrultusunda bilgilerin açığa çıkmasını sağlamaya çalışmaktır. Buna inanmak öylesine bir güçtür ki, hakikatimize ulaşmakta bize engel oluşturacak duygusal etiketleri ve etkilerini silip, yok edebilir.

The inexplicable terror
crawled through my labyrinth of veins
My amygdala rapidly sending confusion
to the faithful drummer in my chest beating
up a strong solo.

~Stella A. (Middle School, 2007-8)

Most of the research available on the amygdala revolves around fear and terror. There are still many unanswered questions. This poem truly captures the mystery and confusion of emotions. Emotional signals travel in our bloodstream, invading many parts of the body including the faithful drummer in our chests. Strong emotions increase blood pressure, creating tension in the heart and giving us the subjective sense that our heart “hurts” when we feel profoundly upset.

In this poem, emotions are portrayed as difficult to explain and highly individualized. It seems that emotions drum up a different beat in each person and serve as a guide for producing some sort of rhythm. Stella composes a wonderful representation of emotions through music, a common form of emotional expression. If emotions are the beats and rhythm to music, then what is responsible for the production of melody and harmony?